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:

[youtube http://www.youtube.com/watch?v=oMAbv0VXxP8&w=560&h=315]

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!

[youtube http://www.youtube.com/watch?v=yinn9APpj7Q&w=560&h=315]

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.

[youtube http://www.youtube.com/watch?v=vYJytyuPDBk&w=420&h=315]

[youtube http://www.youtube.com/watch?v=GUWmiV2azHE&w=420&h=315]

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.

Most of the time when we deal with an acute inversion ankle sprain, we look at how to manage it for 16-18 hours out of the day and maybe add in some elevation at night if there is significant swelling. But could we do a little more to speed the recovery time or at least decrease the discomfort during the night? If the individual with an ankle sprain sleeps on their back or on their side (if they lay on their stomach, this solution will not work), here is something to try to help mediate some of the acute pain with laying on their back/side with an acute inversion ankle sprain.  This mechanism/solution may seem negligible, but I can assure you that your patient will thank you for at least suggesting this as an option.

Although anatomic variations and pre-existing lack of mobility may prevent this from occurring, but for many, when the leg is rested on a surface, such as in supine with the posterior aspect of the calcaneous in contact with the surface, the effect of gravity naturally places the ankle into a bit of plantarflexion.  With plantarflexion, a concurrent anterior glide of the talus occurs which is slightly accentuated by gravity both on the foot and through the talocalcaneal bridge with the tibula/fibula. This is because the calcaneous acts sort of like a fulcrum in which the talus has a relative anterior glide due to the effect of gravity driving the tibia and fibula gently posteriorly  on the talus towards the resting surface due to size and weight differences. As a result, additional stretching/irritation of the anterior talofibular (ATF) ligament may occur. If the patient rolled on the side which places the injured ankle’s lateral aspect to be faced towards gravity, gravity would then contribute to the foot/ankle invert/adducting and minor stretching/irritation of the calcaneofibular (CF) and ATF ligament. Similarly, having the ankles lateral aspect on the support surface, through bodyweight and lack of conformity of the surface, minor stretching/irritation of the CF/ATF ligament may occur.

One way to counteract this kind of stretching/irritation is with a conforming pillow, which can assist with preventing the amount of plantarflexion in supine, and inversion, in side lying which may occur while laying in bed/couch, etc. But a pillow can be more cumbersome and require a fair amount of adjusting throughout the night to accommodate.  Another way is through a small homemade/athletic training room/clinic made supportive device:

Take a simple piece of foam tubing (IE: pipe insulation tubing or thin floatation device) cut it to a length that can cover the back of the ankle and both malleoli. Thread a piece of string through it to allow it to be fastened around the ankle. Tie the string tight enough to allow it to stay on the ankle above the calcaneous at the talotibiofibular joint, but loose enough to easily remove.

This foam supportive device provides support at the talotibiofibular joint which, in supine, reduces the influence of the posterior glide of the tibia/fibula on the calcaneous (reduced relative anterior glide of talus) and also mildly dorsiflexes the ankle. In side lying, it can be positioned more inferiorly to prevents inversion/adduction with the lateral aspect facing to the sky, and left at the talotibiofibular joint line when the lateral aspect of the ankle is facing the resting surface. Basically, we are trying to prevent additional stretching of the soft tissues associated with anterior glide of talus.

In theory, this may secondarily assist with healing, as it helps keep the ATF,CTF, the capsule, and other tissues in an approximated position. This may be beneficial after aggressive posterior talus mobilization/manipulation as well.

…Ofcourse, everything I just described above could be complete hocum and simply the additional sensory contact around the ankle could act like a counter-irritant. Regardless, speaking from experience, it just feels better.

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).

[youtube http://www.youtube.com/watch?v=cPebQCkSLCs&w=420&h=315]

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.

Ever had an external rib torsion which just would not calm down? I had one of these for about 6 months and a fellow student had theirs for several months as well. Addressing the t-spine and the rib itself both through manual and exercise helped a little, but didn’t seem to resolve it completely. Instead, we were both able to treat it successfully with this amazing tool:

Towel

Yes, a towel. We folded a medium sized towel to approximately 1/2 to a 3/4 inch in thickness. This towel was then placed under the painful rib, and slept on. It was positioned in way that whether you slept on your back or on your side it would maintain a constant level of compression on that rib. At first, the intent was just to reduce discomfort of the rib pain at night, but unintentionally, it became the complete treatment and resolved the issue. It took about 4 nights for me and about 10 days for other student. Problem solved. Easy and safe intervention to use concurrently with manual and therex, or possibly try it by itself?

The Rotator (Demonstrating Internal Rotation)The Rotator (Demonstrating External Rotation)

Chris Melton from Joint Mechanix sent me a free trial of the Rotater back in March. When I first received it, there were a few minutes of blank staring at it trying to figure out which way to hold the Rotater to get it to do what I wanted at the moment. When I finally watched the DVD that was enclosed, I had to smirk when Eric Beard also became confused on which way to hold it in the outtakes. Needless to say, like with anything I review, I took my time to play with it for a while before I make too many comments on it. In addition, because I have a bit of excess ROM in both internal and external rotation, I really did not use the rotator much myself. Instead, I had a few individuals with restrictions try it out and merged their thoughts with what I observed while they were using it. So here is the review:

As is usually the case with anything I touch, I tried to turn the Rotater into something other than it was designed to do. I wanted a lot of stretching and strengthening variations, but that is not the point of the Rotater. The Rotater is what it is. Which is not to say that is bad in any way, it is the best at what it is designed for, which is for self controlled stretching into focused internal and external rotation. This is a good thing, because as has been mentioned before, the greatest part of the Rotater really is the ability of the patient to control the stretch themselves. I have never been a fan of assisted stretching, but IR and ER stretching is difficult to do independently, typically requiring assistance. However, this can be risky, as I have seen partner assisted shoulder stretching sessions resulting in strains and even tears. The Rotater design solves that problem by putting the control back into the hands of the individual themselves, making it great for post-op shoulder surgery, pitchers/throwers, and any individual lacking IR and/or ER. The design also allows IR/ER to be stretched in nearly all ranges of shoulder flexion and abduction which can help with designing functional ROM progressions within post-op restrictions. The Velcro band can also be used as a gentle resistance point for self-administering PNF stretches or even oscillating stretches at the end range if the need arises.

I want to clearly state, that when it comes to addressing limitations of ROM, I still believe the first goal should still be address joint mobility of the effected joint and those around it to see if the ROM limitation clears up without more focused stretching. If it does not, there is still an important place for additional stretching, and in the case of lacking IR/ER in the shoulder, the Rotater really shines in this area!

So what were my concerns and dislikes? At first, I was concerned about the durability of the Rotater, but the reality is it survived a couple of incidences of being stepped on, thrown and dropped, and aggressively being flexed. I thought the amount of flex that occurred with stretching and the strong arm would eventually give and snap it in half, but it has held well and Chris stated the flex was actually there by design for durability. Regardless, they warrant the Rotator all the way around, so if anything were to break they would replace it.

One specific dislike I had was mostly to do with my own personal preferences. I just do not do very much focused IR/ER strengthening with most of the people I work with. So for me I was not entirely sold on the strong arm attachment. It worked as it was intended, but it was time consuming to switch between IR/ER. If an individual needed a very specific range to be worked with tremendous control and only in one direction, it could work well. However, I tend to do more stabilization, eccentric control,  and multi-joint/multi-planar exercises for the shoulder. Although you could use it for controlled stabilization and eccentric control, I prefer getting the entire shoulder involved using another method.

Overall, the beauty of the Rotater is in its simplicity, it does its intended job very well. I commend the team over at Joint Mechanix for putting the Rotator together without an orthopedic rehab background!

The Rotater

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.

I was originally going to do a little write-up on Vladmir Janda’s prone hip extension (PHE) test, but I found that Dr. Greg Lehman has already done a great job with the topic on his blog. As Dr. Lehman mentioned, we really don’t know what to take from this test from a research perspective. Clinically, many have seen that this test does demonstrate test-retest changes with a successful outcome in a treatment. In fact, I have observed a clinical example in which a patient with hip pain had been participating in numerous closed and open chain exercise interventions that involved hip extension and hip abduction to address their hip pain with no improvement. Yet, ultimately a single prone exercise which emphasized conscious effort to perform isometric gluteal contraction completely resolved her year long struggle with hip pain. Despite this clinical evidence, little research regarding injury and the gluteus maximus has been performed. I thought I’d do a quick blurb on some of the few studies which have shown some correlation between gluteus maximus activation and any injury.

Bullock-Saxton, Janda, and Bullock demonstrated a correlation between ankle sprain injury and an increased delay in gluteal activation2. Similarly, Bruno and Bagust demonstrated an increased delay in gluteal activation in low back pain (LBP)1. One concern with both of these studies were that they utilized the PHE test, in which Dr. Lehman already pointed out previous research showing inconsistencies in activation patterns including the relevance of the gluteus maximus delay. Further yet, since the PHE is performed in “prone”, we have remember, as Gary Gray likes to point out, everything changes once the foot hits the ground. Vogt and his team examined muscle activation patterns in both an LBP and asymptmatic population during walking. In their study, they demonstrated that both the gluteus maximus and the erector spinae were active for a prolonged period of time in an LBP population and that, oddly enough, the glut max fired earlier (although so did the erector spinae and hamstrings) in the gait cycle than the asymptomatic population5. Likewise, during standing extension from a full flexed position, Leinonen et al. demonstrated that in a LBP population, the glut max  fired earlier than the erector spinae4. So wait, aren’t we trying to get the glutes to fire earlier as a result of our treatment, or possibly even longer, in the thought of protecting the spine? However, research seems to indicate the body is already trying to do it for us.

So here in lies our enigma regarding gluteus maximus activation and our beliefs regarding its role in musculoskeletal dysfunction. Clinically we’re seeing results with what we perceive to be our gluteal emphasized exercise prescriptions, but it might not be for the reasons we think. As Dr. Lehman mentioned, we may be looking at the wrong variable of gluteal function, perhaps it is peak amplitude or glute max endurance3? Or perhaps our treatments are effecting something else entirely, and simply performing a neuromuscular extensor pattern in the “region of dysfunction” is enough to get a therapeutic benefit (a good future blog topic!).  Regardless, we need to be open to alternative explanations for the gluteus maximus enigma, in particular if those explanations come with improved outcomes.

1. Bruno PA, Bagust J. An investigation into motor pattern differences used during prone hip extension between subjects with and without low back pain. Clinical Chiropractic. 2007;10(2):68-80. doi: 10.1016/j.clch.2006.10.002.

2. Bullock-Saxton JE, Janda V, Bullock MI. The influence of ankle sprain injury on muscle activation during hip extension. Int J Sports Med. 1994;15(6):330-334. doi: 10.1055/s-2007-1021069.

3. Kankaanpaa M, Taimela S, Laaksonen D, Hanninen O, Airaksinen O. Back and hip extensor fatigability in chronic low back pain patients and controls. Arch Phys Med Rehabil. 1998;79(4):412-417.

4. Leinonen V, Kankaanpää M, Airaksinen O, Hänninen O. Back and hip extensor activities during trunk flexion/extension: Effects of low back pain and rehabilitation. Arch Phys Med Rehabil. 2000;81(1):32-37. doi: 10.1016/S0003-9993(00)90218-1.

5. Vogt L, Pfeifer K, Banzer W. Neuromuscular control of walking with chronic low-back pain. Man Ther. 2003;8(1):21-28.