We were honored to have Ben Geierman (@medicinal_movement_rx) attend our PSMMT November course and also spend a day observing the application of the course materials in our clinic at Dynamic Movement and Recovery. Ben has taken a number of courses over the years and has really good insight into the global picture of the Biopsychosocial model across the recovery and training paradigm. He was kind enough to write up his experience of the weekend as well as how it was applied in the clinic. We offer this opportunity to any of our course attendees and we believe it gives the most insight to see the content in action. Without further ado, here were Ben’s thoughts:

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This past weekend I had the unique opportunity to not only take Dynamic Principles Pain Science, Movement, & Manual Therapy (PSMMT) course but also to spend the following day with Leonard & David experiencing first hand how they incorporate the principles taught in the course into the everyday application of treating those in pain.

Overall, the course was a great overview of the current evidence on everything pain, manual therapy, neurodynamics, contextual factors, and critical thinking. However, I found myself most intrigued by the lab component and ‘movement experiments’, particularly with walking and standing.  Initially, these movement experiments seemed quite peculiar as I walked back and forth across the clinic, being mindful of the feelings in my feet, ankles, knees, hips, spine, and so forth all the way up to the head. We performed a similar experiment in standing, playing with various stances and positions at each joint to try to find the greatest position of ease. These were very interesting experiments and quite novel to me, however, I wasn’t quite sure how I would implement them in the clinic or honestly if I could even get patients to take them seriously. However, those concerns were quickly resolved as I spent the next day with Leonard and David watching them put these experiments into action.

Both Leonard and David used the movement experiments quite often during treatment sessions and I was surprised to see how well patients responded to them. Most of the patients we saw that day had persistent pain and previous therapy consisting of more structural interventions and passive modalities without much relief. However, the movement experiment approach was much different and allowed the patients to actively explore their experiences. One patient’s experience in particular stuck with me. She was having hip pain and felt it every time she stood up. By leading her through a movement experiment and some mental visualization techniques, she was able to subtly alter the way she moved all by herself and stand up pain free in less than 5 minutes. Another patient with low back pain participated in a walking experiment and was able to become more mindful of her movement and find a way to decrease her symptoms through finding the movement pattern that provided the most ease. Now most of these patients still had symptoms, but by utilizing these movement experiments, they were able to be more mindful of their movement, experience their symptoms, and discover a new way to move in order to “create space” within their experience to allow for more movement freedom and decreased suffering.

The magic of these experiments further solidified their usefulness as I found myself at the gym in the following days. I had personally been working through some knee pain for the past few weeks while simultaneously completing my powerlifting programming in an attempt to increase the strength of my squat. This was beginning to become quite a frustrating experience, as my knee pain would consistently increase in severity as I added weight to the bar, causing me to have to decrease the weight on the bar during my top sets and subsequently cease the progress I had been making before the knee pain arose. However, after spending the weekend at the PSMMT course, I decided to run a little movement experiment myself. By playing with my stance, squat depth, and bar position, I was quickly able to discover a squat pattern that allowed me to squat without symptoms and even work up to my programmed weights on my top sets essentially symptom free.

Now I pride myself on being a ‘movement optimist’ and finding ways to modify painful movements temporarily while sensitivity decreases, but even in light of that, the pain I experienced in my knee over the past weeks and the associated frustration that came along with the inability to progress my strength as planned, narrowed my perspective to the point where I found myself in a repeating loop of pain and frustration.  This essentially incarnated from coming into the gym feeling fairly well, working up to a decent weight, and like clockwork, experiencing a return of pain in my knee pain again. This experience, as I believe is common with many pain experiences and supported the movement variability research, led to me to pigeonholing my options with various squatting techniques due to my hyper vigilance and yearning to perform the movement as usual without any pain. I think this is such a common occurrence with folks dealing with pain, especially persistent pain, where we get stuck in a rut of doing things the same way over and over again without noticing and continually experiencing the same symptoms, creating a vicious cycle or pain that further fuels itself. However, the beauty of the movement experiments is to allow you to find alternative options on your own to break this cycle by improving your relationship and awareness with your body and movement, all while increasing autonomy and self-efficacy by managing symptoms independently.

Overall, this course was a game changer for me and getting to experience first hand how the material was implemented in the clinic was invaluable. Although I took the most from the movement experiments, there were a ton of other gems in the course and nuggets on new research that I had not been aware of and which will certainly positively affect my future practice. Nonetheless, the magic of the movement experiments will stick with me most, and I loved the acceptance and commitment therapy (ACT) framework presented alongside it for working with people dealing with persistent pain. The whole approach is essentially aimed at accepting the symptoms but committing to engage in meaningful activities despite, in order to decrease suffering and improve function. However, it’s imperative to recognize that acceptance does not mean passivity and by using the movement experiments, patients are able to actively create space by becoming more mindful of their movement, leading to greater flexibility to live meaningfully in spite of pain. I firmly believe this approach will be immensely helpful for my future patients dealing with persistent pain and I highly recommend experiencing Dynamic Principles course first hand for any healthcare provider treating humans in pain.

Ben Geierman DPT, CSCS

There is an epidemic of movement professionals emphasizing outcomes without understanding “why” they are seeing the things they are seeing in human movement. Whether a rehabilitation profession, a strength and conditioning coach, or personal trainer, just because something changes, doesn’t mean that it had anything to do with the specifics of what you did, there are many factors involved in movement behavior change, most more powerful than the direct effects of your prescribed exercise! The “why’s” that are frequently touted tend to be focused on rigid structure, failed understanding of tissue strain curves and plasticity, and a fallacy of some sort of predictable patterns which must be re-organized like a puzzle piece or molded like a piece of putty. There is rarely a basic analysis of the underlying physiology that creates the measurable change that is occurring. Failure to investigate the most studied mechanisms for the changes we see, limits significant potential for improving prescription strategies and may also increase risk of harm of the client for which the plan was made. In fact, the education we use to describe our movement strategies may negatively impact the potential of that movement strategy, or even harm the client’s beliefs about themselves and their potential. Furthermore, a failure to understand how psychology, social factors, and culture are tightly interwoven into the physiology of human movement has long term implications of movement across a lifespan.

Below are 8 examples of strong basic scientific concepts related to movement which are vital to understand for anyone who observes and prescribed movement interventions

  1. Flexibility and Mobility
    • Muscles, tendons, and other soft tissues are not independently operating tissues of the body, they cannot become “tight” or “stiff” on their own, they require a nervous system, immune system, and endocrine system (infact there is growing evidence muscle is a an important endocrine organ!) to be able to do anything including how willing they are to move and be lengthened. To understand flexibility, range of motion, and “mobility” you must understand nociception in contexts other than pain. You must understand that nociception does not equal pain and plays a vital role in many areas of human function. If nociception was pain and if we have “pain fibers” and “pain signals” in the body, then we’d all be screaming in pain as we explore our available range of motion, because how nociception is processed is what predominantly regulates your flexibility and your ability to change it. Your nervous system is the primary driver of how willing your muscles and tendons are to lengthen, if it feels you shouldn’t lengthen that tissue, no amount of stretching will change it unless you can “play with processing” to see if it will behave in another manner. Fundamentally, if the term stretch tolerance is new to you, you missing out on the most basic fundamental science of stretching and mobilization, stretch tolerance the cornerstone physiology of range of motion works in humans.  (here, here, here, here, here to start) Furthermore, by understanding stretch tolerance and knowing that nociception is both peripherally and centrally facilitated and modulated means you need to understand a persons thoughts and emotions are going to regulate how much the muscle will resist lengthening. (see here) The amount of time wasted on stretching and mobility activities emphasizing an area that doesn’t want to move is ridiculous. Odds are very good there is a reason the tissue is behaving the way it is, and efforts to try and change it may counteractive to the functional benefits of it being “tight”, perhaps the behavior could even be protective! We see this very clearly with running, if the gastrocsoleus and achilles tendon complex did not stiffen with increased volume of running, you would lose a tremendous amount of passive tissue energy reserve which reduces strain and effort throughout the body. Yet here thousands of runners waste their time “stretching” their calves, or thinking they are mobilizing their talus with a band, fighting against a very useful and performance enhancing adaptation. Worse yet, and depending on the area emphasizes, this excessive time spent on mobility and flexibility may contribute to unhelpful compulsive behavior and potentially result in tissue injury in the long term. Remember, it doesn’t require a fancy technique or tool to change mobility, just play with context and processing and see what happens, look here for an example.
  2. Strength and Durability of Soft Tissues
    • To fail to understand the high tensile strength, adaptability, resiliency of connective tissues and normal connective tissue changes such as scar tissue, means to not understand the purpose and nature of fascia and to not understand tendon/fascia skeletal muscle interface as related to movement.  (here, here, here, here, here)  Fascia really has two primary purposes, it’s a firewall to protect the spread of infection to deeper tissue, and to conserve energy. Take for example the IT band, which requires over 2,000 lbs of tensile force to lengthen a measly 1% in length, that tensile strength is what helps to make walking gait and running far more efficient, it has to be tense! Let alone the basic science of physics clearly indicate you as a clinician could not lengthen it (or any other piece of fascia) even if you wanted to! Over emphasizing and/or under appreciating these fundamental concepts of soft tissue leads to many common time-wasting strategies, promotion of negative self-beliefs, obsessive behaviors, and possible injury to neurovascular structures. Clinically it is not that uncommon I see athletes who regularly “roll their IT band” end up with significant sensitization of the lateral femoral cutaneous nerve, which can sometimes take a very long time to calm down. The warning signs are common, if you find yourself upgrading from a foam roller, to a bumpy roller, to a PVC roller, to a steel pipe and beyond,  because you can’t get your targeted area to “mobilize” like it used to, you are starting to experience some change in nociceptive processing, you are experiencing less the DNIC effect. (Diffuse Noxious Inhibitory Control) DNIC is part of what gives you the illusion of tissue change but is actually an endogenous modifier of nociception and nocifensive behavior such as tissue guarding (see #1 above). Keep ignoring the growing sensitization and thinking the tissue just needs to be “Beat-up more” to be “mobilized” and the problem could expand into something else.
  3. Regional Emphasis on Mobility
    • This is one my most frustrating things to see on social media and I’m equally guilty for previously propagating this misunderstanding in the past.
      • “Focus on dorsiflexion to improve your squat” – No, you don’t need to, dorsiflexion only influences one aspect of a squat, the ability to go past the toes, which you may want if you want more quad work. It’s based on the idea that there is some form of “good” squat form, there is not, you squat the way your body is built, you don’t force your body into a particular squat. The key is, you can still get a great squat with less dorsiflexion, there are thousands of other ways to squat to and past parallel, and ways to work your quads more, all while meeting the ability of your anatomy safely and appropriately. Squat to your anatomy, not into it, or past it!!
      • “Your hip flexors limit your squat” – No, they don’t, look at the anatomy and follow the osteokinematics with the origin and insertion. No, they don’t, please look at the anatomy. Please stop.
      • “Your psoas is too tight and pulling on your back keeping you out of neutral spine during your squat” – No, it isn’t, no it can’t. See above. And no you can’t keep a neutral spine, see below.
      • “Mobilize those hips to get this very specific angle of hip width/ER/flexion in your squat that you must have to protect your spine” – Your hips can only move in the way your anatomy was built. Human hips have a great deal of femoral acetabular variation, it is common and many factors influence it. (see here) Even a form of the “dreaded”  Femoral Acetabular Impingement (terrible name for a normal variant of the body) exists in some manner in up to 67%  of asymptomatic individuals (here) Odds are if you keep pushing hips into a direction where two bones get really close to each other, your body might start to guard or get angry. See topic 1 above for consideration.
  4. Keeping a Neutral Spine
    • Human bodies cannot keep a neutral spine while squatting, even in highly trained Olympic lifters. No matter what, 40-50 degrees of lumbopelvic flexion always occurs during efforts of “maintaining neutral” while squatting or picking something up (see here). If you are worried about spinal flexion and spinal discs, perhaps it’s best to realize we are all “doomed” and maybe that doesn’t matter. Or perhaps our understanding of the biomechanics of the spinal discs is that in weight bearing flexion is not that of a jelly donut, and might protect the spinal cord and nerve roots in comparison to neutral or extension. (see here)
  5. Stabilization and Muscle Activation Exercises
    • Guilty as charged, I sadly even wrote articles to perpetuate this limited concept without fully questioning many of the authors and clinicians thinking. This is the problem when you expect “leaders in the field” to do the critical thinking for you rather than delving into it yourself to make sure what they are saying makes sense. The fundamental problem is there are no specific “stability” motor control patterns written into the body that can be assessed or that need to be trained, there are a number of very fundamental aspects of humans with spines that are commonly missing from the dialog, in particular, the role of context in posture and movement. Rather than “stability” motor programs in the human body; there is a “keep from tipping over”, “don’t drop that thing”, and “don’t get squashed” contextually derived dynamic postural-righting behavior that is heavily influenced by your emotions and your thinking in real-time. (start here and here) Many of the smaller muscles of the spine are spending a good chunk of their time as sensing organs while other portions of their time fine tuning movement with other larger and smaller muscles, sometimes they’re even allowing the passive structures to do work, and that’s normal and needed for the health of the spine articulations and structure – Gasp!  Any effort to train them is an exercise in futility. Every study that has examined this belief shows there is no change in actual muscular behavior when doing specific exercises; doing those exercises might make a person feel better for a number of other reasons, but nothing changed with how the muscles function. (here, here, here, here, here, here to start) Furthermore, things like specific order of activation of muscles, do not exist, I’ll let Greg Lehman take it from here and here. We can’t program motor behavior with exercise prescription, they’re not programmable, you can condition the muscles but their motor behavior is dynamic, not static, and the amount of factors involved in that dynamic state, let alone the infinite numbers of contexts they are changing in, is impossible to predict and accommodate for with a deliberate exercise. Specific “Stability exercises” are not only a waste of time but may reinforce pain related behaviors by reducing variability of the trunk in response to context, which may be detrimental in the long term by creating a virtual “movement prison” (thanks to Jarod Hall for that term).
  6. Emotions and thoughts in Movement
    • If you fail to recognize the vital importance of emotions and thoughts in the human movement, you fail to understand motor behavior in a meaningful way, motor control and coordination does not exist in a sterile environment, in fact their very development is dependent on emotions and cognition. (here, here, here, here,). Trying to make someone selectively “turn-on” (since when was it off??) or emphasize an muscle when they have significant stress in their life is not just a futile effort, but it’s essentially impossible for them to do in that context of their life in that moment. Their motor circuitry is overloaded by their emotional state which no cognitive cue is going to override. Fear results in massive co-contraction of the TVA, multifidi, IO/EO, rectus, and ES! That corset is already there, the problem is, they don’t know how to do anything BUT brace their core at that moment.
  7. Posture is Biopsychosocialcultural
    • If you fail to understand the psychological, social, and culture roles of how humans hold themselves, you do not understand posture, it is not just a bunch of bones stacked on each other. (see previous post on this here)
  8. Injury Prevention is Non-specific
    • There are many “injury prevention” and “bullet-proofing” programs out there by a number of gurus. Some of those gurus were hired by professional sports organizations, how do you think those teams are doing? (here, here, here to start.). When looking at specific vs. general programs of preventing injury, no specific strength, flexibility, or neuromuscular control strategy stood out amongst the rest (here). Simply doing something different than current sport while participating in your sport seems to help, and the slow burn recognition that the most predictive return to sport after injury are psychosocial factors is slowly making it into daylight.

If these concepts are new to you, please take the time to struggle with them. I started this journey toward understanding movement 21 years ago for my own benefit and then began trying to help others 5 years later and I’m still processing this stuff on a daily basis to make sure I can best take care of myself and my clients. There are a lot of unknowns in movement, but as described above there is a strong scientific basis for shifting the way we look at human movement through a Biopsychosocial lens and not getting caught up in this illusion of a “movement system” that operates like a machine. We are not simple cars, we are so much more than machines.

I haven’t updated in a while due to time devoted to opening a new clinic called Generation Care Performance Center.

However, I felt compelled to make a quick, blunt, review of Todd Hargrove’s: A Guide to Better Movement: The Science and Practice of Moving With More Skill And Less Pain. Simply put, this book is the most important book on movement in the last 20 years, possibly in existence up to this point. It will become a required reading for every movement professional to truly understand movement and pain. I have made pitiful attempts to touch on some of the concepts of this book in the past, but Todd has so elegantly written words which convey a clear understanding of the integration of movement in the Neuromatrix, that  I don’t know if I could ever add to it (but will foolish try at some point!). This book is fully accessible to both the clinician and the patient/client. Thank you Todd for your efforts, your clarity, and how incredibly affordable you have made this knowledge in an age of academic inflation. If you don’t buy this book, you are doing a disservice to your patients, and yourself. Buy it now!

*Note: This is part of a series of thoughts on the topic of looking at movement and movement related symptoms as influenced by the nervous system. These will be dynamic posts with additional content and references being added as time allows, but the primary purpose of the posts are to share my current thoughts on the influence of manual therapy and exercise on what we see and feel in our patients. I hope others will engage me in these thoughts and provide their perspectives and also criticism into the process.

In part 1, I wanted to provide the definition for post-antalgic patterning which I believe is important to understand before thinking about how we treat it (if it even needs to be treated), for which I lay the ground work here:

Post-Antalgic Patterning – Part 2 – A Quick Reference for Manual Therapy and the Nervous System

A little over a year ago Jason Silvernail released a great video summary on manual therapy and the nervous system called “Crossing the Chasm” which definitely had its intended effect on me. This discussion has been a “hot topic” for at least a decade. As I have attempted to share this same information with other clinicians, I have noted a trend towards wanting more “practical” connection between the techniques we use on a daily basis and the nervous system. As a result, over the last year I have started to formulate a way to bring a little bit of clarity to a very complex topic.

Mechanoreceptors – The elephant in the room

In most of our academic preparatory programs for various rehabilitation disciplines, our afferent and efferent sensory nerve fiber education has focused primarily on severe neurological conditions of the peripheral and central nervous system (stroke, spinal cord injury, CNS disease, etc.). However, when it comes to the role of the nervous system in musculoskeletal conditions, the focus tends to be on nocioception (note of importance: nocioceptors are NOT PAIN RECEPTORS!), chemoreceptors (in particular the relationship to inflammatory mediators), proprioception, muscle spindles, and the golgi tendon reflex. We might touch on some afferents when we talk about gate control, but in general, mechanoreceptors are a very minor part of “most” professional academic programming offerings. This is despite that fact that mechanoreceptors may be one of the bodies most densely dispersed points of interaction with our nervous system, in particularly in the tissues we commonly claim to be treating (joint capsules, fascia, ligaments, muscles, etc.).

I remember vaguely talking about Ruffini Endings, Merkel’s discs, Pacinian and Meisners Corpuscles, but I don’t remember much emphasis on them and I certainly didn’t see any value in even recalling their names at the time. Yet now I realize they are probably some of the most important structures I deal with on a daily basis, in particular when it comes to manual therapy interventions. We get so obsessed with the biomechanical properties of soft tissue and joints and the illusion that we can mechanically alter them through our hands and various tools despite growing evidence that this simply is not the case, or at best, has an extremely small role in the big picture. Yet we choose to ignore, or at the very least downplay, the one basic fundamental pathway, the cascade of neurophysiological events which occur every time skin is compressed. These events can result both in short term and long term tissue and movement quality changes which have the potential to explain every single “change” seen through the use of manual therapy. Furthermore, any inflammatory, fluid dynamics, or thermal responses which potentially could come about from an aggressive intervention could have chemical, thermal, and fluid interactions with mechanoreceptors, chemoreceptors, and thermoreceptors thereby compounding and/or altering an existing externally induced neurological stimulus. If the inflammatory, fluid, or thermal process remains active for hours or days, this could yield a sustained stimulus on mechanoreceptors, thermoreceptors, and chemoreceptors thereby influence the nervous system for an extended period of time (think of a “built-in portal e-stim unit” that already exists in all humans).

Perhaps more important than the external stimulus itself is the ability to modify, enhance, and/or guide the therapeutic outcome of the neurophysiologic response from the stimulus with an educational context provided to the patient, allowing for a profound impact on how they perceive touch and movement.

So what does the pathway for this manual therapy to mechanoreceptor stimulus to tissue quality/movement change look like? Dr. Schleip has perhaps best described this in his work on fascial plasticity, of which this diagram provides perhaps the most concise explanation of the relationship between manual therapy and the nervous system.

Schleip, R. (2003). Fascial plasticity–a new neurobiological explanation Part 2.Journal of Bodywork and movement therapies, 7(2), 104-116.

Schleip, R. (2003). Fascial plasticity–a new neurobiological explanation Part 2.Journal of Bodywork and movement therapies, 7(2), 104-116.

To further help solidify the connection between our commonly utilized manual therapy techniques and the nervous system, I put together a couple of acronyms to show the connection between groups of mechanoreceptors and various manual therapy technique:

“RuffMerks need tender care”

  • Ruffini Endings (End Organs) & Merkel’s discs are slow adapting mechanoreceptors which respond best to slow sustained and deep tension
  • ANS (PNS) & CNS interactions
  • General massage, myofascial release techniques, and possibly even ischemic trigger point releases likely preferentially engage these mechanoreceptors

“PacMeisners need action”

  • Pacinian and Meisners Corpuscles are fast adapting mechanoreceptors which respond best to fast & vibratory inputs and are key to texture discrimination (think edged/textured tools)
  • Predominantly CNS interactions although ANS (PNS) possible
  • Greater concentration subcutaneously are also more frequent on the tendinous site
  • IASTM style, cross friction (hand or tool), and oscillating techniques likely preferentially engage these mechanoreceptors
  • Also thought to play a role in high velocity manipulation

 “Free nerve endings do it all”

  • Some free nerve endings are intermediate adapting mechanoreceptors and can respond to any form of touch, or any modality (chemical, thermal, electrical) for that matter.

 “Ligamentous Mechanoreceptors – I got nothing”

  • 4 types, varying adaptability, primarily stretch mediated, although possibly facilitated through touch if the ligament is superficial enough to be compressed
  • Engaged primarily with mobilization/manipulation

Last but not least, how can so called “inert” soft tissue, or fascia, have tissue tension or “tonus”?

Smooth muscle fascia copy

More regarding the existence of smooth muscle cells within fascia can be found here.

To be continued in part 3..

*Note: This is part of a series of thoughts on the topic of looking at movement and movement related symptoms as influenced by the nervous system. These will be dynamic posts with additional content and references being added as time allows, but the primary purpose of the posts are to share my current thoughts on the influence of manual therapy and exercise on what we see and feel in our patients. I hope others will engage me in these thoughts and provide their perspectives and also criticism into the process.

Post-antalgic Patterning – Part 1 – A Definition
Injury occurs either acutely or cumulatively. A threshold is reached and threat is detected, whether conscious or unconscious, the body wants to protect itself. As a part of the physiologic chemical cascade of events which occurs in an attempt to address the potential structural damage, the nervous system, both central and peripheral, protects the region through numerous responses including localized guarding or splinting. This guarding process involves contractile activation of muscle AND the CONTRACTILE activation of what has previously been defined as inert soft tissue, such as fascia, joint capsules, ligaments (1). As a result, kinematics, arthrokinematics, and tissue dynamics may be altered and movement may change. Some of it is subtle, some of it not (2). Regardless, it appears that occasionally, this alarmed state stays active long after the tissue has healed and the threat removed (3).

Steering away from the complicated matter of pain, better discussed in Explain Pain, I wish to focus on what I call “post-antalgic patterning”. This is the existence of an altered movement pattern that is most often an unconscious behavior that remains long after an injury has been healed, or possibly even perceived injury. It exists anywhere in the body with any movement, not just gait! This pattern is a chronic pattern, which begins as early as 2 weeks after an acute injury and remains a minimum of 6 months or for a multitude of years. It may be associated with patient symptoms through regional interdependence, or it may not. Post-antalgic patterning may resolve spontaneously or it may best respond to touch and/or movement coaching. In this definition, any clinician perceived “dysfunction” of the joint or soft tissue contributing to this movement pattern is propagated by the nervous system, not structural change and is minimally influenced by joint or tissue inflammation or swelling.

This pattern may or may not be mechanically inefficient, and it may, or may not, further propagate future episodes of threat elsewhere in the body. In truth, it may just be what it is. Perhaps changing it makes functional improvements and improved symptoms, perhaps not. This is key, because we really don’t understand it, and we have to know when to just ignore it and have the patient move on with life despite this perceived asymmetry, because in reality, we do not know if it might have always been present. This is important, because you have to put limits on how much you try and attempt to alter, as the concept of a “symmetrical” human is fairly illogical. Rather, the objective is to simply to provide an environment to allow movement in a way that the patient can regain trust in these areas, to become more active, which is where the healing occurs.

Your hands or tools aren’t magic. They may or may not be appropriate to providing that supportive environment for altering this pattern, but if you use them, realize their sole purpose is to get the patient moving, reducing threat and letting the tissue re-accommodate to activity.

To be continued in part 2..

1.) Schleip, R., W. Klingler, and F. Lehmann-Horn. “Active fascial contractility: fascia may be able to contract in a smooth muscle-like manner and thereby influence musculoskeletal dynamics.” Medical hypotheses 65.2 (2005): 273-277.

2.) Crosbie, Jack, Toni Green, and Kathryn Refshauge. “Effects of reduced ankle dorsiflexion following lateral ligament sprain on temporal and spatial gait parameters.” Gait & posture 9.3 (1999): 167-172.

3.) Gribble, Phillip A., et al. “The effects of fatigue and chronic ankle instability on dynamic postural control.” Journal of athletic training 39.4 (2004): 321.

The EDGE series

As indicated in my review of the EDGE series of tools and the fact that I am a re-seller of the EDGE (my disclaimer), I am a huge advocate of Instrument Assisted Soft Tissue Mobilization (IASTM) in terms of providing a different neurophysiological input in comparison to using your hands and reducing the amount of stress you place on your hands with soft tissue treatment techniques. I have found that with practice I can accomplish similar within session changes in ROM, strength, and symptoms as other manual techniques. At the same time, I question the rational of using tools to promote tissue healing and to break down scar tissue. I believe this approach has promoted far too aggressive treatment in the past, and at this time, we really do not have great evidence to support this philosophy of treatment. I hope this post provides some insight into why I have this concern.

What is the evidence for IASTM use?

While I believe IASTM to be a valuable tool in my rehabilitation arsenal with its own indications and limitations of use, there are some who have purported tools as being downright magical in their abilities to “heal” patients. Some major brands claim 80-100% success rates for nearly every musculoskeletal condition under the sun, but record and maintain these records privately, available on request only. From the published experimental study realm, far less data is available.

To date, only one randomized controlled trial in humans has shown a better outcome using a tool over hand based manual therapy intervention.  Wilson et al. (1) compared cross friction (using hands) to IASTM on individuals with patellar tendinitis. 20 subjects (12 men & 8 women) were randomly assigned to either the IASTM group (10 subjects) or the hand cross friction group (10 subjects) with both groups having the same standardized therex and modality interventions. The IASTM group had 8 treatments over 4 weeks and the cross friction group had 12 treatments over 4 weeks. Full resolution was considered having no swelling, no pain upon palpation, and minimal pain (<3/10) performing six single leg hops, squatting to thigh parallel, and performing an eccentric load step down. Clinical evaluation and self-reported questionnaires were completed at 0, 6, and 12 weeks.  Based on their full resolution criteria, at 6 weeks 10/10 subjects in the IASTM group had 100% resolved symptoms  and 6/10 in the cross friction group had full resolution. The remaining 4 from the cross friction group was crossed over to IASTM to be re-assessed at 12 weeks with 2 additional subjects accomplishing the full resolution criteria established by the researchers.

Only two other experimental studies have examined IASTM as an intervention. Burke, et al. (2) compared IASTM to soft tissue mobilization with hands on carpal tunnel syndrome and found that both were equivocal to each other. Blanchette et al. (3) compared IASTM to education, ergonomics, and stretching on lateral epicondylitis, IASTM by itself was found to have no greater or earlier improvements than the control.

Numerous level 2 evidence case reports and case series studies that examined IASTM have demonstrated favorable outcomes in isolation and after other interventions had failed.(4-9) However, as is the nature of these studies, they provide no insight on the mechanism or whether another intervention may have been just as beneficial.

From my personal perspective, I am not looking for magic and I have no concern whether outcomes using a tool may be equivocal to my hands or other interventions(2,3), because at the very least I know it does have a therapeutic effect. This now assures me that I can give my hands a break from time to time and be more willing to experiment a variety of patients using the stimulus of the tool as option, potentially identifying an individual who may be more positively responsive to the tool than you had previously assumed.

Can IASTM help with tissue healing?

Two of the largest names in IASTM make numerous claims regarding the tissue healing and “regenerating” ability of their IASTM tools and techniques. They both have webpages which claim amazing research evidence for their philosophy of treatment. Sadly, little of this “evidence” is available for public consumption. A quick glance at this list shows that only 3 studies on rats provide any insight on the role of IASTM in tissue healing. I will separate many of the popular claims of tissue healing into 3 categories to review the literature: Activate the histamine response and increase local inflammatory response, break down scar tissue and/or re-arrange some nondescript “fibers”, and increasing fibroblasts to the region.

Activate the histamine response and increase local inflammation

Oddly, although erythema is the most obvious effect noted clinically with IASTM, this is not something that is well studied. I have only been able to find one study which utilized Gua Sha to examine micro circulation. (10) The comparison of Gua Sha to IASTM is difficult to make because Gua Sha is significantly more aggressive than most forms of contemporary IASTM.  Gua literally translates “to scrape or scratch” and Sha can best be described as “red, raised,millet-size rash”. As shown below, it is extremely traumatic looking:

Gua Sha Treatment - NOT A GOAL OF IASTM!

I personally would never want to do anything like this one of my patients. With that in mind, the results of the study demonstrate that, shockingly, yes local superficial circulation is increased when you scrape the tissue.  However, this was after 7.5 minutes of aggressive treatment, which is far more than the average IASTM protocol. Furthermore, the circulation increases were noted as superficial, which questions the ability to infer increased nutrient delivery to, or removal of waste from, deeper muscle, tendon, or other soft tissue.

On a side note to those of us that are neurophysiologically minded, this study also examined Gua Sha’s effect on decreasing pain. After treatment, decreased pain was not only noted locally and regionally but also in  areas far distal from the treatment region. This finding made the authors themselves question the relevance of increasing local circulation for the purpose of pain relief. But I digress…

Scar Tissue (Type III collagen) break down and “realigning fibers”

So what about the idea of breaking down scar tissue or realigning fibers? Loghman and Warden examined IASTM on experimentally induced MCL injuries in rats. (11) They did not specifically address the soft tissue breakdown or “fiber realignment” but did note that “There were no grossly observable differences between ‘IASTM’ treated and non-treated ligaments at either 4 or 12 weeks post-injury; however, non-treated ligaments often had more adhesions and granular tissue, and were more difficult to harvest than IASTM-treated ligaments.” which to date is the only experimental discussion of tissue adhesions related to IASTM.

I will note that Dr. E has reported that a colleague of his is completing a ultrasound imaging study which notes changes in the fiber quality after 2-3 minutes of IASTM treatment. Since this study is still being prepared for publication, at this time I have not been able to review the results.

This is one area I would love to see evidence for tissue change, and I believe there is a “slim chance” for us to scrape “adhesions” surrounding superficial paratendons and tendon insertions around our distal extremities (ie: achilles tendon and insertion).  However, it is important to keep in mind that when we feel the “grittiness” or “adhesions” under our tools, we really don’t know what we are feeling. We cannot say with certainty that it is scar tissue we are feeling. We forget that way back in the day during cadaver dissection we used to see a lot of fatty tissue and non-deformable soft tissue adhesions subcutaneously which could easily explain what we are feeling. Further more, often times after several sessions of treatment, these “adhesions” rarely change, only the tissue tension and tonicity we originally aimed for changes. BUT, there are times that these “adhesions” do disappear after treatment, and I would like to know more about that.

Despite all this, I will not deny that secretly in the back of my head I would love to believe that me scraping paratendon sheaths is breaking up longitudinal “scar tissue” (type III collagen) and promoting movement of the sheath and therefore the tendon, but I recognize simple muscle activation and movement probably breaks up as much “scar tissue” as anything I am trying to do to the tendon with the IASTM tool.

Promoting Collagen Synthesis by increasing fibroblasts proliferation

rat

Increased fibroblast proliferation has been the only consistently demonstrated histological property of IASTM. (11,12,13) Although this has only been noted in rats.  Furthermore, Gehlsen et al. demonstrated that increased pressure from the tool resulted in greater fibroblast proliferation. (13) However, what the value of increased fibroblast proliferation is in the long term has not been demonstrated. Loghman and Warden’s rat MCL study showed that although the IASTM group had greater improvements in healing early on, by the 12th week, there were no histological differences in healing between treated and untreated rat MCLs.

And that’s it, that is all we know regarding tissue healing and regeneration related to IASTM. From evidence in rats only, we can promote fibroblast proliferation, but even in the rat studies, when compared to tissue healing without IASTM, no difference is noted after 12 weeks of healing.

Conclusion

Personally, I do not think the tissue healing concepts will pan out any better in future research, nor do I care if it does or not. It is too easy to fall into the “tissue quality” trap, where we chase the make-believe picture of “good quality tissue”, rather than looking at objective measures which are rapidly changeable to meet the patient’s functional goals. As with any manual therapy intervention, I am primarily interested in within and between session improvements which allow me to promote movement to get the patient moving which is ultimately the only thing that will change tissue. If IASTM helps tissue healing, it’s a bonus, but I do not want it to be focus of my treatment or my education.

I want to end this post with reference to a recent study by Alfredson, et al. which examined the most extreme version of tissue scraping, surgical scraping under anesthetic, in the treatment of chronic achilles tendinopathy. (14) In their study, they recruited only individuals with bilateral chronic achilles tendinopathy, and surgical scraping was only performed on one side (the most painful side). Despite having expected to need a second surgery for the opposite side, 11 of the 13 patients had full resolution of symptoms bilaterally after unilateral scraping. Many already had full satisfaction bilaterally within the first 6 weeks. The authors make a good discussion why they believe these improvements were centrally mediated, not mechanically oriented. It is an excellent read and well worth the time locating.

The Sales Pitch

With the understanding that many of the systems out there have little published evidence for the unique benefits of their expensive educational programs that they require you to complete in order for you to be able to purchase their IASTM tools. Why not consider one of the lowest cost options on the market with the best ergonomics, inclusion of all the most popular concavities and convexities (multiple tools in one), and no entry level requirements available in both stainless steel and plastic? Check out the EDGE and EDGEility series of tools!

1.) Wilson JK, Sevier TL, Helfst RH, Honing EW, Thomann AL. 2000. Comparison of rehabilitation methods in the treatment of patellar tendinitis. Journal of Sports Rehabilitation. 2000;9(4): 304-314.

2.) Burke, et al. 2007. A pilot study comparing two manual therapy interventions for carpal tunnel syndrome. Journal of manipulative and physiological therapeutics 30(1):50-61.

3.)Blanchette, Marc-André, and Martin C. Normand. 2011. Augmented soft tissue mobilization vs natural history in the treatment of lateral epicondylitis: a pilot study. Journal of Manipulative and Physiological Therapeutics 34(2):123-130.

4.) Slaven EJ, Mathers J. Management of chronic ankle pain using joint mobilization and ASTYM® treatment: a case report. Journal of Manual and Manipulative Therapy. 2011;19(2):108-112.

5.) Davies CC, Brockopp DY. 2010. Use of ASTYM® Treatment on Scar Tissue Following Surgical Treatment for Breast Cancer: A Pilot Study. Rehabilitation Oncology. 28(3):3-12.

6.) McCrea EC, George SZ. 2010. Outcomes following augmented soft tissue mobilization for patients with knee pain: A case series. Orthopaedic Physical Therapy Practice. 22(2):69-74.

7.) Hammer, W.I., Pfefer, M.T. 2005. Treatment of a case of subacute lumbar compartment syndrome using the Graston technique. J Manipulative and Physiol Ther. 28:199-204.

8.) Hunter, G. 1998. Specific soft tissue mobilization in the management of soft tissue dysfunction. Man Ther. 3: 2-11.

9.) Melham TJ, Sevier TL, Malnofski MJ, Wilson JK, Helfst RH. 1998. Chronic ankle pain and fibrosis successfully treated with a new non-invasive augmented soft tissue mobilization technique (ASTM): A case report. Medicine & Science in Sports & Exercise. 30(6):801- 804.

10.) Nielsen, Arya, et al. 2007. The Effect of Gua Sha Treatment on the Microcirculation of Surface Tissue: A Pilot Study in Healthy Subjects. EXPLORE: The Journal of Science and Healing. 3(5):456-466.

11.) Loghman, M.T., Warden, S.J. 2009. Instrument-Assisted Cross-Fiber Massage Accelerates Knee Ligament Healing. JOSPT. 39(7):506- 514

12.) Davidson, C.J. Ganion, L.R. Gehlsen, G.M., Verhoestra, B. Roepke, J.E., Sevier, T.L. 1997. Rat tendon morphologic and functional changes resulting from soft tissue mobilization. Med Sci Sports Exerc. 29: 313-319.

13.) Gehlsen, G.M., Ganion, L.R., Helfts, R. 1999. Fibroblast responses to variation in soft tissue mobilization pressure. Med Sci Sports Exerc. 31: 531-535.

14.) Alfredson, H., Spang, C., & Forsgren, S. (2012). Unilateral surgical treatment for patients with midportion Achilles tendinopathy may result in bilateral recovery. British Journal of Sports Medicine. Epub Ahead of Print. Nov 28.

Furniture sliders are extremely inexpensive (less than $10 at Lowes) and extremely versatile. I was inspired by Ross from Ross Training to experiment with these tools. One of my favorite exercise progressions is a multi-planar single leg squat. The slider is a great cue to promote mobility and stability as well as adding flow to a sequence of movements. It easily allows progressions and regressions based on the needs of the individual.

This is part 3, the last of a series of posts reflecting on some highlights in learning about movement that I experienced in this last year. In part 1, I addressed my experience with Applied Functional Science / Chain Reaction™ Biomechanics and presented an application of this approach using hip internal rotation. In part 2, I reflected my current thoughts on strength and conditioning. Now in part 3, I discuss my thoughts behind Fascia, Anatomy Trains, and Regional Interdependence.

Much of what we thought we knew about the biomechanical science of fascia and myofascial release is bunk. By saying this, I need to make it clear in advance that this does not change how we treat, rather it changes how we educate our patients and perhaps makes you think more critically about why you might, or might not, want to treat in a certain way. Greg Lehman provides an excellent review of fascial science on his blog.

fascia-man

So what about Anatomy Trains, which I have previously stated may be a beneficial overview for regional interdependence? As Dr. Lehman discussed, it is extremely unlikely that from a manual therapy standpoint we are making biomechanical changes to tissue. If anything, the biomechanical representation of Anatomy Trains better represents fascial adaptation to function and will only respond to progressive overload with daily stresses and exercise. Furthermore, if we look at function and movement, “Form Follows Function” , then the representation presented by Anatomy Trains may vary individually because tissue adapts to the stresses induced on a daily basis.

So we need to throw out the patterns presented by Thomas Meyers, correct? I personally do not think so. This is not the first time we have developed a general map which is not truly accurate of an individual representation. Our good friend the cortical homunculus also is an inaccurate representation of the somatosensory cortex.

Homunculus1

Why? Because the brain is plastic and the somatosensory cortex adapts to how we interact with the world over time, which is most clearly demonstrated by cortical reorganization in phantom limb pain. Yet we still can use the homunculus as a general representation to give us a visual to for understanding sensation. Similarly, I still believe that seeing the patterns in Anatomy Trains can help us better see movement globally and therefore help guide treatment with complex patients representations. From a movement perspective, especially globally, we need to have some way to compartmentalize all the information and how they approximately relate to each other. Joint by joint osteokinematics and arthrokinematics help but can get complex quickly when you combine them with muscles and fascia. Patterns, such as those represented by Anatomy Trains, which encompass both bone and soft tissue, can help compartmentalize and make treatment more efficient if used appropriately. Of course, the reverse is also true, chasing patterns religiously will also take away from the most obvious, efficient, and appropriate treatment approach. Needless to say, these patterns do manifest themselves in our clients and patients from time to time, and to be ignorant of their general representations will cost you and your patient time.

As a side note, we are in a new era of our understanding of pain, with increasing emphasis on a neurophysiological role in this picture. There may be some overlap between the cortical homunculus and fascial adaptation over time. Since fascia is highly innervated with Ruffini and Pacini corpuscles, changes in fascia from physical adaptation to stress and from habituation to particular forms of movement may influence sensory perception and could theoretically be represented in the somatosensory cortex. With some recent evidence regarding the possible existence of a nocioceptive map which overlaps closely with the somatosensory cortex, there is the possibility that sensory rich fascia may be the interface that allows some of our voodoo with regional interdependence to occur, and why sometimes, specificity matters. This is purely hypothetical, but some ground work for the role of fascia and tendon pain (including pain referral) and their related cortical representation  is discussed by Dr. William Gibson (His PhD thesis is available here: Pain sensitivity and referred pain in human tendon, fascia and muscle tissue.) But since we don’t have any other explanation for how manual therapy sometimes requires specificity and sometimes those points of specificity fall in the patterns represented by Anatomy Trains, this is where I am resting my patient education for the time being.

For a better summary than what I wrote above, I highly recommend a post by Alice Sanvito titled:  “If we cannot Stretch Fascia, what are we doing?”.

Sometimes I forget how long the debate over abdominal hollowing (drawing in) vs. bracing has been going on. We’re close to 20 years on this topic. A year and half ago I started writing a clinical commentary on a herniated lumbar disc rehabilitation protocol which included addressing this very topic. A recent resurgence in interest regarding core stability (I guess it never really goes away) made me want to pull an excerpt from the article before it is published. I believe there is a time and a place for abdominal hollowing and abdominal bracing, but there is also a time for neither. The “neither part” has further been bolstered by my experience with Gary Gray’s Applied Functional Science (See Learning about Movement – Part 1). Here is the excerpt:

“Selective recruitment of the TA and multifidi utilizing “abdominal hollowing” or “drawing in” has been described in the literature and is widely practiced. (88,90) In contrast, the simple “abdominal bracing” exercise is another common exercise which not only emphasizes TA and multifidi recruitment, but has demonstrated recruitment of other musculature of the abdominal wall including the internal and external obliques.(89,91) Hodges et al.(85) have demonstrated, using an in vivo porcine model, some increased intervertebral stiffness utilizing TA activation by replicating “hollowing”, more recently, authors have demonstrated that this increased stiffness from “hollowing” is significantly less than during “abdominal bracing” due to decreased activation of the remainder of the abdominal wall musculature. (91,92) When sudden posterior trunk perturbations are introduced, abdominal bracing yielded significantly greater cocontraction of the trunk musculature, increased trunk stability, and better resistance to lumbar displacement than abdominal hollowing.(93) It also appears that the greater the conscious effort utilized to activate the muscular wall, the greater the decrease in spinal stability.(94) Abdominal hollowing has been shown to cause sufficient inhibition of the erector spinae and other musculature to decrease anterior pelvic during hip extension.(95) Inhibition of the erector spinae may have specific therapeutic and treatment benefits in addressing potential muscular imbalances, however they are valuable contributors to stable functional movement, which may result in decreased pelvic control if inhibited.

Although cocontraction of the TA and multifidi has been perceived as vital for muscular stabilization of the lumbar spine, their attempted selective activation may decrease anteroposterior trunk stability,(91-94) theoretically placing rotational trunk stability at risk through decreased activation of the external obliques in comparison to abdominal bracing.(89,91) Despite this, utilizing “hollowing activity” in the early in treatment phases of treatment can provide some symptom relief, kinesthetic awareness, motor control education, and provide some early activation of the TA and multifidi during the acute phase. However, once an individual progresses to postures that involve weight bearing, utilization of bracing may be better to enhance multiplanar stability.

Ultimately, conscious efforts towards bracing and/or hollowing do not contribute toward functional stability, rather, focus should be redirected towards addressing specific motor patterns utilizing multiple muscles in order to develop comprehensive spinal stability.(96) Moreover, from a theoretic functional perspective, consciously constraining movement in any region of the body over an extended period of time may alter the demands placed upon numerous other regions of the body. This may be best illustrated with the influence of external fixation, such as the use of a spinal orthosis for reducing pelvic mobility,(97) single segment spinal fusion influencing segmental motion around it,(98) and the increased risk of degeneration above and below the segment of lumbar fusion.(99) Although these examples entail extreme measures of stabilization beyond the level produced consciously by an individual, it serves as a reminder that a balance between mobility and stability is necessary to enable responses to the dynamic demands during movement of the human body.”

85. Hodges P, Kaigle Holm A, Holm S, et al. Intervertebral stiffness of the spine is increased by evoked contraction of transversus abdominis and the diaphragm: In vivo porcine studies. Spine (Phila Pa 1976). 2003;28(23):2594-2601. doi: 10.1097/01.BRS.0000096676.14323.25.
88. Richardson CA, Jull GA. Muscle control – pain control. what exercises would you prescribe? Manual Therapy. 1995(1):2-10.
89. Richardson CA, Snijders CJ, Hides JA, Damen L, Pas MS, Storm J. The relation between the transversus abdominis muscles, sacroiliac joint mechanics, and low back pain. Spine (Phila Pa 1976). 2002;27(4):399-405.
90. Hides J, Wilson S, Stanton W, et al. An MRI investigation into the function of the transversus abdominis muscle during “drawing-in” of the abdominal wall. Spine (Phila Pa 1976). 2006;31(6):E175-8. doi: 10.1097/01.brs.0000202740.86338.df.
91. Grenier SG, McGill SM. Quantification of lumbar stability by using 2 different abdominal activation strategies. Arch Phys Med Rehabi. 2007;88:54-62.
92. Stanton T, Kawchuk G. The effect of abdominal stabilization contractions on posteroanterior spinal stiffness. Spine (Phila Pa 1976). 2008;33(6):694-701. doi: 10.1097/BRS.0b013e318166e034.
93. Vera-Garcia FJ, Elvira JL, Brown SH, McGill SM. Effects of abdominal stabilization maneuvers on the control of spine motion and stability against sudden trunk perturbations. J Electromyogr Kinesiol. 2007;17(5):556-567. doi: 10.1016/j.jelekin.2006.07.004.
94. Brown SH, Vera-Garcia FJ, McGill SM. Effects of abdominal muscle coactivation on the externally preloaded trunk: Variations in motor control and its effect on spine stability. Spine (Phila Pa 1976). 2006;31(13):E387-93. doi: 10.1097/01.brs.0000220221.57213.25.
95. Oh JS, Cynn HS, Won JH, Kwon OY, Yi CH. Effects of performing an abdominal drawing-in maneuver during prone hip extension exercises on hip and back extensor muscle activity and amount of anterior pelvic tilt. J Orthop Sports Phys Ther. 2007;37(6):320-324.
96. Kavcic N, Grenier S, McGill SM. Determining the stabilizing role of individual torso muscles during rehabilitation exercises. Spine (Phila Pa 1976). 2004;29(11):1254-1265.
97. Konz R, Fatone S, Gard S. Effect of restricted spinal motion on gait. J Rehabil Res Dev. 2006;43(2):161-170.
98. Schwab JS, DiAngelo DJ, Foley KT. Motion compensation associated with single-level cervical fusion: Where does the lost motion go? Spine. 2006;31(21).
99. Putzier M, Hoff E, Tohtz S, Gross C, Perka C, Strube P. Dynamic stabilization adjacent to single-level fusion: Part II. no clinical benefit for asymptomatic, initially degenerated adjacent segments
after 6 years follow-up. Eur Spine J. 2010;19(12):2181-2189. doi: 10.1007/s00586-010-1517-4.

This is part 1 of a series of posts reflecting on some highlights in learning about movement that I experienced in this last year. I hope to be able to do this on an annual basis as a record of self-reflection and hopefully provide some value to others out there on the same journey.

Applied Functional Science / Chain Reaction™ Biomechanics

SKBK_WuShu_Aerial_R

I have previously discussed my interest in going more in depth into multiplanar movement with my posts on 3D stretching as well as regional interdependence. I have used the FMS and SFMA off and on for a few years and felt they were both efficient and useful for their respective purposes, and I love that the research community is actively exploring the validity and reliability of these tests. I will still utilize components of these tests from time to time. However, I have personally found I need to change to a more customized approach to evaluation. In the past, I have found that in the middle of testing, I would break out of the protocols established trying to “tease” out something that did not fit cleanly into any of the tests. Part of this is just my nature, I have a difficult time adhering to standardized procedures and the way I do things just kind of evolves and varies depending by how I perceive something is presented to me. As these breakout sessions grew in complexity, I knew that for me personally I needed to explore some other philosophies which probably have figured out things I have yet to even think to ask about. Gary Gray’s Applied Functional Science (AFS) was the first approach that peaked my interest after that point. Gary Gray arguably pioneered much of the functional training movement, with Gray Cook stating publicly he has been strongly influenced by Gary Gray’s thought process. However, getting to the point of wanting pursue learning about the AFS approach has been a 4 year journey. When I first watched videos of Gary demonstrating and discussing his thought process, I completely disregarded it because my bias at the time of what I was seeing was an awful amount of poor quality movement with no regard for what is currently considered stability, in particular with movement of the spine. But over time, I could not deny that this freedom of motion looked more useful than I had first thought. I finally bit my lip and jumped in, eventually realizing I need to at least give it a try. It was probably one of the best decisions I could have made and now has significantly influenced how I view movement and exercise prescription.

I was given the opportunity to be exposed to the AFS approach through a nine week clinical rotation at Shoreline Sport & Spine in Spring Lake, MI. There are currently 6 Fellows of Applied Functional Science™(FAFS) at this location. A FAFS has completed a 40 week fellowship through Gary Gray’s Applied Functional Science (AFS) approach. The clinicians at Shoreline have integrated AFS with a wide variety of manual therapies and other interventions which was a fantastic eclectic experience that allowed me to explore a number of ways to integrate this philosophy.

Before presenting on this topic, I must first acknowledge that these are my personal reflections on the experience, and if they are in error, they should not reflect upon the excellent clinicians at Shoreline Sport & Spine. I am certain more than one FAFS will perceive I might have missed the boat on key points, and to that, I respond that I plan to formally take a Chain Reaction™ course in the future to see what else I might have missed. Furthermore, I am commenting on but a drop in the ocean of what the AFS system entails. The “Functional Nomenclature” alone requires a 44 page manual to address simply the language and fundamental principles. That being said, here are some key things I learned from this experience:

“Drivers facilitate chain reactions throughout the body”

This was the earliest, most applicable, concept I learned from my exposure to the AFS/Chain Reaction model. It may seem like a simple statement but it is incredibly profound when broken down even a small amount. Rather than simply thinking about one joint moving on another and leaving it at that, the Chain Reaction model demands that every joint be examined from a proximal on distal and distal on proximal perspective, what are the joints above and below doing, and what planes of motion (sagital, frontal, transverse) all of the joints are moving in during any musculoskeletal action. Central to this is the concept that during movement, a driver leads the movement and the joints above and below follow that same movement, but at different speeds as they progressively move in the direction dictated by the driver. This delay in speed/timing of a bone following another bone is the Chain Reaction explanation for much of what we understand about arthrokinematics. When bones move on top of each other in multiple planes of motion in the various representations of roll, glide, spin, etc.,  they are doing so according to the congruencies afforded to them to allow them to follow the next bone and joint as led by the driver.

In most of our manual therapy courses, we examine relative motion of one joint on another and addresses joint movement in various planes of motion based on arthrokinematics. Traditionally, looking at joints this way was left to the manual therapy realm and not the exercise prescription realm. Oddvar Holten likely made the earliest attempt to merge the manual therapy perspective with exercise prescription with his Medical Exercise Therapy (MET – Not to be confused with muscle energy technique) which focused on utilizing various apparatuses to isolate spinal segmental levels and extremities and then focusing on patient induced movement into one or more planes of motion specific to the desired outcome determined in the manual therapy diagnosis. The Chain Reaction approach more broadly addresses this by including concepts more similar to regional interdependence and primarily using the patient’s own body and extremities to control the levels of segmental or joint emphasis through prepositioning such as: Holding on to a stable or unstable support, modifying the weight bearing surface (wedges, angles, instability), conscious prepositioning, etc. It then utilizes another joint or point of the body above or below (could be FAR above or below) to facilitate movement at the joint in the plane, or planes, desired. This approach is both a diagnosis and a treatment, which is the focus of the AFS approach. It integrates extremely well with existing manual therapy interventions, or in Gary’s opinion, independent of traditional manual therapy models, resulting in him developing his own manual therapy system specific to the AFS called Functional Soft Tissue.

Getting back to the idea of a “driver”. A driver is anything which “drives” motor behavior. This could be any part of the upper extremity, lower extremity, trunk, neck, head, eyes, sense organs, and/or even fears and beliefs. The driver itself has numerous variables which can be applied to it: Is it open or closed chain based? What action is performed? What is the direction of movement? What is the speed? What are the force demands? Etc. etc.. This is just a small list amongst many other variables, not even addressing fears and beliefs.  The entire process can get very complex, very quickly, when broken down in the nomenclature which requires looking at every movement from the perspective of:

  • What environment is it occurring in (given available, or specified with certain controls on stability)?
  • What is the beginning position (upright, seated, kneeling, prone, supine, sidelying)?
  • What exactly is the driver (hand, knee, foot, pelvis, trunk, shoulder, etc)?
  • What is the triangulation (direction/target)?
  • What is the action (squat, lunge, reach, pull, etc)?
  • What is the ending position?

I am not qualified to go into that sort of detail, so instead I will provide a broad overview with a contemporary example. Many of us are already applying general versions of this thought process, but do not realize how far we can take it. I will use the example of a kettlebell swing.

 Kettlebell Swing

If you give a new client a kettlebell and only cue them to swing the kettlebell, they will instinctively “drive” the motion using the arms and shoulders, not their hips as you may have originally intended. They do this because you just gave them a cue which facilitates a motor pattern to accomplish the goal in the simplest way the brain understands, which is to swing their arms to swing the kettlebell, rather than to accomplish the exercise prescription goal you had intended, which was likely hip extension. If you change the cue to “Drive the hips forward”, you changed the driver of the motion to the hips, rather than the arms. Now in order to produce the force to swing the kettlebell, the individual will use a hip extension strategy. You just changed the entirety of the neuromuscular patterns utilized, even though you had the exact same exercise setup. Change the driver and the motor behavior changes.  Now, if you expand this to joint by joint, things get really interesting.

Take for example working mobility and stability of hip internal rotation. There are a handful of non-weight bearing activities which involve the femur actively or passively internally rotating on the pelvis.

ch158f14

We may begin with a manual therapy intervention to address mobility, then provide a mobility exercise, then a stretch, then we prescribe an exercise for stability, then we address another joint which may be associated, and we give it a mobility exercise, and a stretch, and a stabilization exercise, on and on we go. We may end up providing a large amount of exercises, all of which take time, with very specific cues and details to remember. Now with AFS, if we apply the concept of a driver along with any number of subtle changes, or “tweaks” as Gary likes to call them (the process is called “tweakology”), we can tailor a custom exercise specific to our patient needs across multiple joints with reduced need for extensive cuing and details. This can be done with fewer exercises overall because we can integrate mobility, stability, and movement across multiple joints, in multiple planes of motion, into simple exercises which require less time for the patient perform. Progression and regression are simple to teach because you are using movement patterns the client/patient already knows, you simply tweak one or two components to make changes towards the movement you want to improve.

As I am already far over my target word count for this post, I will finish with a video in which I discuss some basic strategies to emphasize hip internal rotation in weight bearing and function: