*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.

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?”.

Back in August, a group of authors, van den Bekerom, et al. published an article in the Journal of Athletic Training which reviewed the evidence for the use of RICE in acute ankle sprains1. The authors concluded that, other than some extremely limited and low quality evidence for ice, there is very little evidence for rest, compression and elevation. The most interesting to me, and purpose of this post, was the discussion of rest, which I felt the was best summarized from the article itself: “All included studies had a similar conclusion: some type of immediate posttraumatic mobilization is beneficial in the treatment of acute ankles sprains“. And curiously, although this was a team of medical doctors writing this article, it appeared that form of mobilization was preferentially (not directly stated) manual therapy.

Although I have not had a chance to do a thorough follow-up lit review myself (always a good practice in reviewing systematic reviews), based on references selected by these authors, it appears there is more published evidence (regardless of quality) towards the use of manual mobilization/manipulation2-6 than activity/exercise7-9. Of particular interest was an examination by Eisenhart, Gaeta, and Yens6, which  examined the use of manipulation (fibula, talocrural, cuboid, and anything else clinically determined), soft tissue techniques (fibularis/peroneals, etc.), and lymphatic techniques combined with RICE (with or without pain meds) in comparison to RICE alone (with or without pain meds) in an emergency department. The group which received manual therapy demonstrated decreased pain, decreased edema, and improved dorsiflexion/plantar ROM (ROM was not statistically significant though) compared to group that received RICE alone. Since it typically does not get more acute than patients showing up at the emergency department, I felt this was a great study to demonstrate the value of manual therapy for acute ankle sprains. Combined with evidence that long term restrictions in posterior talar glide post ankle sprains4, there is clearly evidence for some form of early manual therapy in most inversion ankle sprains.

Despite recognizing the increased risk of compensation injury and general increased risk of injury from deconditioning, RICE, in particular rest and relative immobilization, remains the mainstay for the acute inversion ankle sprain. It is my belief (and I am sure many others) that this treatment philosophy needs to change at every level of patient care, and I believe athletic trainers and physical therapists need to lead the way. Although consideration for the individual patient should be made, as a general guideline, if we are presented with a patient with an acute inversion ankle sprain, our thought process needs to move away from the “rest/immobilization” component unless there is a clear need. Obviously “RELATIVE REST”, ie: not return to full sport participation may be a short term need, but full immobilization and crutches for the purpose of non-weight-bearing is likely unnecessary and potentially harmful. Instead, once a fracture or significant traumatic instability is ruled out, make the foot and ankle move, both actively and passively, and ideally with full weight bearing. Clearly if an excessively antalgic gait is present and cannot be resolved with manual therapy, tape, or other modalities, an assistive device may be necessary to improve the quality of gait, but ambulation with gait training to avoid compensation should occur early.

For those who prefer guidelines towards directing treatment, Whitman, et al. 10 developed a CPR for predicting whether thrust, non-thrust manipulation, and exercise in acute inversion ankle sprains could improve outcomes. They were able to determine that the presence of 3 out of 4 variables: Symptoms worse when standing, symptoms worse in the evening, navicular drop greater than or equal to 5.0 mm, and distal tibiofibular joint hypomobility were present; are predictive of dramatic improvements with a 95% success rate in treatment outcomes if manual therapy and exercise interventions are utilized.

To drive home these points I have 2 recent cases I want to share to demonstrate the clinical value of manual therapy in the management of an ankle sprain. Case 1 involves a 55 year old female who recently experienced an acute ankle sprain after waking up in a recliner and getting up rapidly, not realizing her left lower extremity had “fallen asleep”, resulting in a significant inversion of the left ankle and a “not so graceful” landing onto the floor. Initial evaluation revealed she was positive for 3 of 3 of the Ottawa ankle rules, so she was referred for X-ray. X-ray was cleared, she was provided crutches, and she presented to me 16 hours post injury with significant swelling and difficulty weight bearing. I performed distal fibular head mobilizations and talocrural mobilizations which result in immediate visible decreases with swelling without the involvement of any lymphatic techniques. Furthermore, it allowed the patient to weight bearing with 80% decrease discomfort. Additional soft tissue treatments of the peroneals and lateral aspect of her gastroc allowed her to ambulate without an antalgic gait, and without the crutches she arrived with. Although she still reported some mild discomfort, she was able to be off her crutches from that point on. I was able to see her for 2 sessions before she was sent on her own with 90% improvement within a week after her initial sprain. I would have liked to continue to work on the foot ankle, but she was private pay and she was satisfied with the improvements she already had, I discharged her to HEP with self mobs and progressive strengthening and instructions to keep moving. Clearly I can’t say if these outcomes would have been any different had she been partial-weight bearing for a week or more, but I can say that I was able to produce immediate functional improvements which improved the quality of her life sooner rather than later.

Case 2 is a story of me, jumping for a Chinese flying lantern stuck in a tree, not realizing on return to the earth my ankles would need to accommodate to a muddy ditch with a 75 degree decline in a very short amount of time. Unfortunately, they did not accomplish this goal and I crumpled like a sack of potatoes with the right ankle significantly inverted under my collapsing body. Of course I had just read this article from van den Bekerom, so I got right up and tried to avoid limping for the rest of the evening. Keep moving and it will just resolve itself right? Well nearly 2 months later of working through it, doing occasional self mobs or having someone do a talocrural manips, I still had episodes after training or moving where there were a few minutes that I could not weight bear pain free without significant pain on the lateral plantar surface and partially through the mid-foot  In the back of my mind I kind of thought this may be something cuboid related because this was a typical presentation for it, and I somewhat proved it to myself that I got the most relief when I attempted a self mobs of the cuboid using a small kobble tool, but it never lasted. It was not until I had learned that one of my fellow PT students, Nan Hannum had recently been trained in the Dr. Allyn Peelen (a local podiatrist) method of cuboid mobilization that I finally had it formally treated. Although I always have a hard time believing in a “systematic” or sequential approach to mobilization, I have seen and experienced great results with Dr. Peelen’s method of treating cuboid and all sorts of vague ankle/foot  issues that did not resolve with other manual interventions. So I thought, why not have her try it on me, especially  since it had been consistently problematic and interfering with my activity levels. With one treatment, followed by a foam bolster taped under the cuboid to “hold the treatment”, I was 80% percent improved. We repeated that treatment 2 days later, second bout of tape, this time 90% improvement. I took the tape off 3 days later, and was able to run 2 days later for the first time in 2 months (Thanks Nan!). Furthermore, that specific pain has not been back since (although I did tweak my talocrural recently of course). Needless to say, the purpose of this case study was  that I personally believe that if I had the talocrural and the cuboid (along with anything else clinically relevant) mobilization the first week, I would probably never have to wait 2 months to get full relief and I probably would not have developed subtle hip pain secondary the subtle antalgic gait. Yes, from an evidence based perspective that is a stretch, but when you see the acute benefits (regardless of the mechanism) of manual therapy with numerous patients, it is hard not to make the judgment that earlier treatment may have prevent later complication.

So with my rambling out of the way. I leave you with a slew of videos of my favorite ankle mobs. First off, you can’t go wrong with Dr. E’s collection of eclectic strategies to improve ankle mobility:

Second, don’t forget the cuboid whip, personally I have had good experience with this with patients, but as demonstrated with the Peelen cuboid sequence, we probably don’t need to be this aggressive because this can be painful!

Finally, I was able to track down two videos of Dr. Allyn Peel himself both performing and using a plastic model to explain his approach to cuboid/foot ankle mobilization.

Oh, and one last thing, don’t forget about the other 6-8 hours of an acute ankle sprain..

References

1.) van den Bekerom, Michel PJ, et al. What Is the Evidence for Rest, Ice, Compression, and Elevation Therapy in the Treatment of Ankle Sprains in Adults?. J Athl Train 2012;47(4):435-443.

(2.) Bleakley CM, McDonough SM, MacAuley DC. Some conservative strategies are effective when added to controlled mobilisation with external support after acute ankle sprain: a systematic review. Aust J Physiother. 2008;54(1):7-20.

(3.) Green T, Refshauge K, Crosbie J, Adams R. A randomized controlled trial of a passive accessory joint mobilization on acute ankle inversion sprains. Phys Ther. 2001;81(4):984-994.

(4.) Denegar CR, Hertel J, Fonseca J. The effect of lateral ankle sprain on dorsiflexion range of motion, posterior talar glide, and joint laxity. J Orthop Sports Phys Ther. 2002;32(4):166-173.

(5.) van der Wees PJ, Lenssen AF, Hendriks EJM, Stomp DJ, Dekker J, de Bie RA. Effectiveness of exercise therapy and manual mobilisation in acute ankle sprain and functional instability: a systematic review. Aust J Physiother. 2006;52(1):27-37.

(6.) Eisenhart AW, Gaeta TJ, Yens DP. Osteopathic manipulative treatment in the emergency department for patients with acute ankle injuries. J Am Osteopath Assoc. 2003;103(9):417-421.

(7.) Karlsson J, Eriksson BI, Sward L. Early functional treatment for acute ligament injuries of the ankle joint. Scand J Med Sci Sports. 1996;6(6):341-345.

(8.) Brooks SC, Potter BT, Rainey JB. Treatment for partial tears of the lateral ligament of the ankle: a prospective trial. Br Med J (Clin Res Ed). 1981;21;282(6264):606-607.

(9.) Bleakley CM, O’Connor SR, Tully MA, et al. Effect of accelerated rehabilitation on function after ankle sprain: randomised controlled trial. BMJ. 2010;340:c1964. doi: 10.1136/bmj.cl964.

10.)Whitman, Julie M., et al. Predicting short-term response to thrust and nonthrust manipulation and exercise in patients post inversion ankle sprain. J Orthop Sports Phys Ther 2009,39(3): 188-200.

A few months ago I talked about the Gluteus Maximus Activation Enigma and the conflicting information obtained on the glute max in the clinic versus what has been demonstrated in literature. It has been difficult for me to address this because I too was guilty of really perpetuating the idea of “gluteal inhibition” and that your “glutes are shut off”, when the evidence for these theories does not exist unless you have a true nerve lesion. It may seem like semantics to the some, but the reality is that our patients and clients take these words very seriously. In fact, I would say a good chunk of them catastrophize the fact that their “glutes aren’t working” and likely worsen the associated symptoms involved in the hip extension dysfunction. I think for athletes in particular to be told that something isn’t working in their body is detrimental to performance for individuals with certain psyches, a point which Vern Gambetta really drives home with his opinion on corrective exercise. At the same time, even if the glutes truly are not “Turned off” or “Firing in the wrong order”, clinically, they are clearly not working very efficiently either, especially if they are significantly asymmetrical. Therefore to find middle ground, I like to look for solutions which help the client/patient remain independent while still participating in their sport even if some form of dysfunction exists by using self evaluation and treatment. I previously mentioned my suspicion that muscle fatigue, rather than muscle inhibition or activation order, may play a part in why our glute emphasized treatments result in reduction of symptoms. A recent article from Hong-You Ge, et al.1 demonstrated that latent trigger points have measurable effects on muscle fatigue made me want to revisit fatigue in the evaluation and treatment of general hip extension dysfunction.  However, I’m going to broaden this idea even further (I’m once again breaking my own rules regarding excessive extrapolation of a research study by doing so) by first looking at addressing the antagonists to hip extension, the hip flexors, prior to attempting to address trigger points/restriction in the gluteals.

I want to preface this write-up to make it clear that I have no evidence for the process that I am about to describe and I am certain there are at least 10 other ways to independently evaluate hip extension. I think both Stuart McGill and Bret Contreras have touched on the use of  different types of bridges in determining hip extension dysfunction in the past, but I couldn’t find the articles offhand, so here is my take on it.

I use a 15-20 rep range of single leg bridges for the patient/client to subjectively identify whether they feel a perceived difference between sides relative to fatigue, ease, and whether it feels disproportionately loaded on the hamstrings, possibly even painful if that is their primary complaint. Then, based on which side is perceived as more challenging, we slightly butcher the classic Janda lower cross syndrome2 and just associate hip flexor involvement with gluteal function rather than look at his original cross of abs to glutes.We’ll generalize it even more and call the hip flexors over active antagonists with possible active or latent trigger points in them decreasing performance of the agonist hip extensors just to integrate the Hong-You Ge et al. 1 discussion a little more.

So for the patient to independently treat this, we start with them attempting to inhibit the hip flexors through a 30 second static stretch for and then retest the bridges. They don’t have to go all the way to 20 reps but they should just be able to go 2-3 more reps more and perceive the exercise as easier. If it does improve, have them do a full minute of static stretching of that hip flexor followed by 3-4 sets of 15-20 reps of single leg bridges to reinforce the more efficient hip extension pattern.  If it doesn’t improve, or they feel only a little better, try a self-TFL release next. Use 1-2 minutes of self release on a tennis ball followed by the same 3-4 sets of single leg bridges discussed earlier.  If they still don’t feel an improvement, go for the glutes directly with a self release. If it works, follow the same pattern of reinforcement from earlier. If there is no change, there is a slim possibility they simply need to train that side more aggressively in hip extension. If this is the case, then we want to have them work on quality reps of single leg bridging on a daily basis for the same pattern of reinforcement as described above. If within one week of working this pattern they still find a single set is fatiguing, the problem does not lie specifically in the hip musculature and it is going to require a bigger picture perspective and likely more involved manual therapy (starting with a pelvic/lumbar eval).

A couple of notes: First off, verify that the fatigue is not just related to the position of their foot and whether they are driving from the heel versus the toes because this can significantly impact loading of the hamstrings between sides.  Second, I recognize not every one of our clients and patients can even do a single leg bridge, let alone 20 of them, but this test and these self-treatment options is not for those individuals anyway. Third, by the 3rd set of bridges, if they’re not used to doing these bridges, they’re going to be fatigued anyway, just do a couple reps for them to subjectively evaluate any chance in the performance of hip extension.

Finally, I admit I am probably still going to use the terms gluteal inhibition from time to time, but I swear I’ll do my best to not give patients or clients the anecdote that their glutes are “shut off” again.

***Update 6/24/12: A great example of when self treatment for hip extension dysfunction fails and more involved manual therapy is needed  from Bill Hartman is found here on his blog.

1. Ge H, Arendt-Nielsen L, Madeleine P. Accelerated muscle fatigability of latent myofascial trigger points in humans. Pain Medicine. 2012:no-no. doi: 10.1111/j.1526-4637.2012.01416.x.

2. Janda V. Muscle strength in relation to muscle length, pain, and muscle imbalance. International Perspectives in Physical. 1993:83-97.

The FDA dictates specific uses and indications of a drug based on pharmaceutical trials. These specific uses and indications are “on the label”. Physicians frequently utilize pharmaceuticals “off label” from their branded purpose based on clinical reasoning. This is a legal and widely accepted practice and necessary to treat conditions which at this time may not have the research evidence available to support the practice but has demonstrated good clinical outcomes. The advent of Clinical Prediction Rules (CPR) and subclassifying of conditions towards specific treatment protocols has been growing in the physical therapy realm5,8,12,13. This is particularly true with manual therapy and CPR for joint mobilizations/manipulations for the cervical, thoracic, and lumbar spine. In general, these guidelines tend to be region specific, IE: a lumbar manipulation for a lumbar condition5,8and cervical spine mobilization/manipulation for neck pain12. Although not as well known, predictive factors for the influence of cervicothoracic manipulation on shoulder pain10 and lumbopelvic manipulation in patellofemoral pain syndrome9 have also been proposed. You could say that the advent of CPRs/classifications is the rehabilitation world’s attempt at providing an “on label” guideline for treatment. However, little other attempt has been made to provide subclassifications for conditions and treatments regarding manual therapy interventions on extremity conditions. Clinically, worldwide, many movement professionals treat extremity conditions one to two joints proximally or distally, in particular through addressing mobility at the spine. This practice is based in the idea of regional interdependence, or “the concept that seemingly unrelated impairments in a remote anatomical region may contribute to, or be associated with, the patient’s primary complaint.”18 In an essence, this practice is “off label”, but unlike the pharmaceutical practice, it is not widely accepted and frequently questioned. This is particularly true from a medical billing and, depending on the location, referral/medical prescription level. Even from within our profession itself, it is not terribly uncommon for the concept of regional interdependence to questioned and perceived as a “wild goose chase around the body” 18.  As I have mentioned in previous posts, Thomas Myer’s Anatomy Trains based system KMI, Gray Cook’s SFMA and Gary Gray’s Chain Reaction Biomechanics™/GIFT Fellowship are perhaps the first to develop standardized evaluation and treatment methods of looking at the body globally rather than locally. Although the terminology varies between each, all of these programs have essentially provided a road map towards understanding regional interdependence. I have minimal exposure to all of these programs, so I cannot give justice to any of them trying to give additional details from their models. However, I wanted to share my thoughts on regional interdependence based on the experience I have gained through my mentors, research, and my limited full-time clinical experience thus far.

A JOSPT guest editorial by Wainner, Whitmann, Cleland, and Flynn titled Regional Interdependence: A Musculoskeletal Examination Model Whose Time Has Come (Freely available directly from JOSPT) written in 2007 probably first popularized the term “Regional Interdependence”, because very little literature prior to this date utilized this term. This editorial presented a great case, both from a clinical and a research perspective, that the practice of examining musculoskeletal conditions beyond the single joint/primarily complaint area is woeful inadequate to address the needs of both common and complicated conditions 18. Research has increasingly been supportive of regional interdependence. Improved pain scores and functional outcomes have been demonstrated painful shoulder conditions as a result of the use of cervicothoracic and rib manipulation 2,4,10,15. Similarly, lumbar and pelvic manipulation has demonstrated improvement in patellofemoral pain syndrome9,16,19. Beyond manual therapy, evidence for the use of foot orthotics for various lower extremity injury as a preventative measure7 and as a method of treating PFPS 17.  However, the role of distal contributions, or more specifically excessive pronation, was recently questioned in a systematic review by Chuter and Janse de Jonge6. In their review, they proposed that a greater influence on lower extremity injury arises proximally from the “core”6. Regardless, what is evident in available research is that proximal and distance regions to the site of injury have some role either as a result of the injury, or as a precursor to the injury1,6,11,14.

Clinically, there are presentations and treatments related to regional interdependence which are a long way (if ever) from being able to be demonstrated or clearly explained in a research design. We are still in the early stages of understanding manual therapy, let alone regional interdependence. Bialosky, et al. (Open access link) provides a great review and proposed a model which encompasses both joint and soft tissue mobilization/manipulation 3.  Although the emphasis of this model and much of the research on manual therapy is based on a neurophysiological, peripheral, spinal, or supraspinal mediated mechanism 3, it is difficult to extrapolate whether these the neurological models also play a key role in regional interdependence. Perhaps now, with the treated “dysfunction” one or more joints away from the injury location, the importance of “movement”, as biomechanically dictated, plays a more important role? Or perhaps still, somewhere in “homunculus land”, a map of regional interdependence is now changed to alter both pain and movement patterns. It is too early to tell, but hopefully this question will soon answered! Whatever the mechanism may be, clinically, there still appears to be a degree of specificity and clinical reasoning necessary in order to provide an optimal outcome. To illustrate this, I want to present a brief clinical case.

This case involves a 23 year old male competitive soccer player who originally presented with posterior left rib pain around T5 region which somehow evolved into some form of left posterior shoulder pain and restricted ROM. Somatic dysfunctions for the thoracic spine, ribs, scapula, glenohumeral capsule, and surrounding tissue(including an incredibly tight latissimus dorsi) were identified. These factors were assumed to be key to recovering the 10-15 degree loss of shoulder flexion with a painful posterior “pinch” at the endrange. A gambit of joint mobilizations and attempts to lengthen the latissimus dorsi, as well as, various techniques for “releasing” other soft tissue restriction was started.  Despite 4 sessions of valiant attempts to regain this loss of shoulder flexion through manual therapy and stretching even up to two joints away, little progress was made. Out of shear randomness, I observed an obscurity in the way the inferior aspect of his rib cage moved when I passively flexed his left shoulder. Perhaps it was an illusion generated by my mind from years of staring at Thomas Meyer’s Anatomy Trains, but something made me believe it was worth looking at his rectus abdominis. Needless to say, simply palpating the rectus abdominis was enough to generate a startle response similar to a typical trigger point presentation. Tension and “restriction” was felt through the lateral band of the rectus abdominis. Much to the patient’s dismay, I spent two minutes “releasing” this restriction and without any other treatment. Immediately afterward, I was able to move him into those last 10-15 degrees of shoulder flexion pain free. One additional treatment was scheduled and the patient was set for a one week recheck, at which point they were still symptom free and discharged.

Looking back now, I could pretend I know what happened and propose a theory to explain it from a biomechanical model utilizing Anatomy trains. I could state that since the rectus abdominis inserts on ribs 5-7, it must then pull on the fascial origins of the pectoralis minor directly or through pulling the rib cage down. Consequently, the pec minor then pulls on the coracoid process of the scapula, which could  result in anterior tilting of the scapula, and therefore give a possible mechanical cause for the “pinching sensation” and  restricting shoulder flexion. The honest truth is, I don’t know why it worked, because it was such a random find. Yet oddly enough, it seemed as though I had to be specific enough in my treatment approach in order to get a positive outcome for this patient. Simply addressing classic restrictions around the shoulder was not enough in this case, I had to go even farther, and I had to use soft tissue! Did I truly decrease the tension in the rectus abdominis and therefore produce the mechanical cascade which lead to this resolution? Could it have been placebo, was the shear randomness of the treatment approach a psychological effect that somehow modulated the pain or ROM changes? I am completely open to any suggestions!

Clearly not every case needs to be this involved or complicated, and sometimes the area of injury is the best place to focus your treatment and leave it at that. At the same time, both clinical and research evidence seems to be paving way the importance of remembering that the leg bone is connected to the knee bone, and the knee bone connected to the thigh bone…

1. Berglund KM, Persson BH, Denison E. Prevalence of pain and dysfunction in the cervical and thoracic spine in persons with and without lateral elbow pain. Man Ther. 2008;13(4):295-299. doi: 10.1016/j.math.2007.01.015.

2. Bergman GJ, Winters JC, van der Heijden GJ, Postema K, Meyboom-de Jong B. Groningen manipulation study. the effect of manipulation of the structures of the shoulder girdle as additional treatment for symptom relief and for prevention of chronicity or recurrence of shoulder symptoms. design of a randomized controlled trial within a comprehensive prognostic cohort study. J Manipulative Physiol Ther. 2002;25(9):543-549. doi: 10.1067/mmt.2002.128373.

3. Bialosky JE, Bishop MD, Price DD, Robinson ME, George SZ. The mechanisms of manual therapy in the treatment of musculoskeletal pain: A comprehensive model. Man Ther. 2009;14(5):531-538. doi: 10.1016/j.math.2008.09.001.

4. Boyles RE, Ritland BM, Miracle BM, et al. The short-term effects of thoracic spine thrust manipulation on patients with shoulder impingement syndrome. Man Ther. 2009;14(4):375-380. doi: 10.1016/j.math.2008.05.005.

5. Childs JD, Fritz JM, Flynn TW, et al. A clinical prediction rule to identify patients with low back pain most likely to benefit from spinal manipulation: A validation study. Ann Intern Med. 2004;141(12):920-928.

6. Chuter VH, Janse de Jonge XA. Proximal and distal contributions to lower extremity injury: A review of the literature. Gait Posture. 2012. doi: 10.1016/j.gaitpost.2012.02.001.

7. Collins N, Bisset L, McPoil T, Vicenzino B. Foot orthoses in lower limb overuse conditions: A systematic review and meta-analysis. Foot Ankle Int. 2007;28(3):396-412. doi: 10.3113/FAI.2007.0396.

8. Flynn T, Fritz J, Whitman J, et al. A clinical prediction rule for classifying patients with low back pain who demonstrate short-term improvement with spinal manipulation. Spine (Phila Pa 1976). 2002;27(24):2835-2843. doi: 10.1097/01.BRS.0000035681.33747.8D.

9. Iverson CA, Sutlive TG, Crowell MS, et al. Lumbopelvic manipulation for the treatment of patients with patellofemoral pain syndrome: Development of a clinical prediction rule. J Orthop Sports Phys Ther. 2008;38(6):297-309; discussion 309-12. doi: 10.2519/jospt.2008.2669.

10. Mintken PE, Cleland JA, Carpenter KJ, Bieniek ML, Keirns M, Whitman JM. Some factors predict successful short-term outcomes in individuals with shoulder pain receiving cervicothoracic manipulation: A single-arm trial. Phys Ther. 2010;90(1):26-42. doi: 10.2522/ptj.20090095.

11. Reiman MP, Weisbach PC, Glynn PE. The hips influence on low back pain: A distal link to a proximal problem. J Sport Rehabil. 2009;18(1):24-32.

12. Schellingerhout JM, Verhagen AP, Heymans MW, et al. Which subgroups of patients with non-specific neck pain are more likely to benefit from spinal manipulation therapy, physiotherapy, or usual care? Pain. 2008;139(3):670-680. doi: 10.1016/j.pain.2008.07.015.

13. Slater SL, Ford JJ, Richards MC, Taylor NF, Surkitt LD, Hahne AJ. The effectiveness of sub-group specific manual therapy for low back pain: A systematic review. Man Ther. 2012;17(3):201-212. doi: 10.1016/j.math.2012.01.006.

14. Souza RB, Powers CM. Differences in hip kinematics, muscle strength, and muscle activation between subjects with and without patellofemoral pain. J Orthop Sports Phys Ther. 2009;39(1):12-19. doi: 10.2519/jospt.2009.2885.

15. Strunce JB, Walker MJ, Boyles RE, Young BA. The immediate effects of thoracic spine and rib manipulation on subjects with primary complaints of shoulder pain. J Man Manip Ther. 2009;17(4):230-236.

16. Vaughn DW. Isolated knee pain: A case report highlighting regional interdependence. J Orthop Sports Phys Ther. 2008;38(10):616-623. doi: 10.2519/jospt.2008.2759.

17. Vicenzino B, Collins N, Cleland J, McPoil T. A clinical prediction rule for identifying patients with patellofemoral pain who are likely to benefit from foot orthoses: A preliminary determination. Br J Sports Med. 2010;44(12):862-866. doi: 10.1136/bjsm.2008.052613.

18. Wainner RS, Whitman JM, Cleland JA, Flynn TW. Regional interdependence: A musculoskeletal examination model whose time has come. J Orthop Sports Phys Ther. 2007;37(11):658-660. doi: 10.2519/jospt.2007.0110.

19. Welsh C, Hanney WJ, Podschun L, Kolber MJ. Rehabilitation of a female dancer with patellofemoral pain syndrome: Applying concepts of regional interdependence in practice. N Am J Sports Phys Ther. 2010;5(2):85-97.