Some time ago, a question came up in the member discussion forum at FixYourOwnBack.com as to whether extruded lumbar disc herniations “went away” or whether they remained in the epidural space. This coincided with an older paper (Haro, 2000) that was discussed on Facebook as the potential mechanism for resorption of extruded disc fragments. I thought that would be a good topic to flesh out a bit with a literature search. I’ll attempt to summarize my reading of the past 13 years of investigation into this topic.

In direct response to the above question, “Yes, resorption of the extruded herniated disc fragments is part of the natural history of disc injury.”  The amount of time that takes to happen varies from person to person but here are a few cullings from several studies:

• Follow up MRI 6-12 months after initial injury demonstrates about 50% of patients see about 70% decrease in size of extruded material. (Fagerlund, 1990, Maigne, 1992, Bush, 1992; Jensen, 1996; Autio, 2006; Monument 2011)
• In a retrospective cohort study, Saal and Saal demonstrated that lumbar disc herniation with radiculopathy can be successfully treated nonoperatively, with nonoperative treatment resulting in “good to excellent” outcomes for approximately 90% of patients. (Saal, 1996)
• MRI findings lag behind improvement of leg symptoms (Ito, 1996)
• Larger extrusions and sequestrations are more likely to resorb. (Maigne 1992, Bush 1992, Jensen 1996)

That last point is interesting as all too often patients report to me that their neurosurgeon suggested surgery because to the large size of the herniated disc fragment. This is somewhat understandable as often a large herniation can cause not only chemical irritation of the nerve root (due to inflammation) but also mechanical compression of the nerve root.  Often intense pain in the leg accompanies this scenario and sometimes motor weakness as well. Years ago, more than 3 days of  progressive motor weakness in these cases drove the clinical decision to decompress the nerve surgically. These days, this 2011 review article sums it up the current “gray” zone we are in…

“In the absence of serious neurologic deficits or for persistent non-radicular low back pain, consensus whether surgery is useful or not has not yet been established. Furthermore, the timing of the intervention with respect to prolonged conservative care has not been evaluated properly.” (Jacobs, 2011)

In their review of randomized controlled trials comparing various interventions for herniated lumbar disc injury with sciatica Jacobs, et al found that after 1 year, there was no difference between surgical vs. conservative interventions. The primary benefit in surgery was quicker relief of the leg pain, with average time before resolution of leg pain averaging 4 weeks in quick surgical interventions, vs. 12 weeks for conservative care.

For those who opt for conservative care and want to know how they can help the process of resorption of the herniated disc material, we are still learning what those variables are. One clear thing to not do is smoke. Tsarouhas et al in 2011 showed that smoking resulted in more severe pain with disc injury, longer time for resorption of herniated disc material and smokers have a longer duration of symptoms.

Many might wonder what the actual mechanism is for resorption of an extruded disc. That discussion gets a bit technical with histochemistry and biochemistry. For those that are interested, let’s “suit up” and get to it!

The Role of Macrophages and Matrix Metalloproteinases (MMPs) in Disc Resorption

Remember those Pac-Man-like things under the microscope in cell biology class that were called macrophages? As it turns out, these differentiated white blood cells (WBC) play a key role in the process.  In a very amoeba-like fashion, they sidle up to the extruded annulus and get to work with a toolbox of cytokines and proteolytic enzymes. Some of these macrophages are residents in a normal disc; others arrive if blood vessels in the outer third of the annulus or in the vertebral endplate are disrupted. The more blood vessels that are disrupted, the more macrophages that are on the scene. While we’re still learning a lot about this process, it resembles a lot of other common inflammatory cascades. Among the enzymes that the macrophages bring that have been studied a bit more, are the matrix metalloproteinases (MMPs)

You can hear the music in your head now, can’t you?

At present, about 24 of these proteolytic enzymes have been discovered and they come not only from macrophages but also from chondrocytes in the disc. I like to think of the different MMPs as different types of cleaners you might use around the house. Maybe you use 409 to clean your kitchen counters, Windex to clean your windows, Clorox to brighten your white clothes and Tide to clean the color garments. Some of those cleaners in certain combinations might not be a good idea for health (ammonia in the Windex + bleach=chlorine gas) and we’ll discuss that analogy a bit more in a minute. Also, you might be able to get a really dirty window cleaner with 409, but Windex will be superior to get the job done. You get the drift?

So those 24 MMPs have been divided up into groups depending on their function.

1. Collagenases (MMPs-1, -8, -13 and -18)– the only enzymes that can cleave intact interstitial collagen molecules.

2.Gelatinases (MMPs-2 and -9)–degrade denatured collagen molecules and basement membrane collagens.

3. Stromelysins (MMPs-3, -10 and -11)– cleaves cartilage matrix components, including aggrecan, proteoglycans, and fibronectin.

4. Membrane-type MMPs (MMPs-14, -16, -17 and -18)–responsible for the activation of other MMPs, but only play a secondary role in direct matrix degradation.

One interesting finding is that a few of these MMPs are present in low quantities in even normal and young discs. As the disc shows signs of increased degeneration, the amount of MMPs and the variety of MMPs increases.

So, if MMPs are needed to clean up a herniated disc, then more must be better…right? Well hold on sparky. These are catabolic proteins, they break stuff down. We have known since the late ‘90s that they are present in greater quantities in degenerated discs, and some suspect that their very presence is the CAUSE of the disc degeneration. As in most bodily reactions, a catabolic agent has an anabolic partner and homeostasis is maintained when we balance those reactions. It seems that when the scale tilts toward the catabolic agents, that’s when we see increased disc degeneration. At least that’s what the correlational studies suggest. Of course you can’t extrapolate causation from a correlation. It could be that the upregulation of MMPs is reflective of a response to injury (essentially a normal inflammatory response) rather than being the cause of the observed degeneration.

You have these inside of you right now. That’s probably OK. Probably.

Current investigations into MMPs are attempting to manipulate the ratio of catabolic MMPs vs. anabolic agents. Some are also investigating the lifestyle issues that are correlated with  low back pain, disc degeneration and with upregulation of certain MMPs. Among those lifestyle items that have been associated with higher levels of degeneration and with higher levels of MMP in the disc is hard physical labor, especially when it involves frequent lifting. The researchers often infer that that lifting equates only compressive load without regard to other vectors of load like torsion and shear. Adams demonstrated to us in 1982 that even in vivo discs are remarkably resistant to pure compressive force but they prolapse with additional flexion + compression. I personally think that an area worthy of investigation is in HOW the disc is compressed. Most of the studies I’m aware of infer compressive load by lifestyle questionnaires looking for employment that involves heavy physical loading of the discs. Some of that sample likely lifts with maintenance of the lumbar lordosis and some likely don’t. I suspect that those that don’t with the inherent flexion + compression moment on the disc, will experience more LBP and more disc degeneration. Indeed, I have noted for years the presence of habitual lumbar hinging (flexion + compression) with naïve and loaded movements toward the floor. Correction of this lumbar hinge by training a hip hinge stereotype has proven to be a remarkably simple intervention to help these painful backs improve.

This does not have a happy ending.

In regards to disc resorption, what are we left with? The natural history after disc herniation is for resorption to occur at varying speeds and degrees dependent on a variety of other lifestyle factors. If you want to improve the resorption process, don’t smoke, exercise moderately but limit heavy physical labor. We still have more investigation to do on the specifics of dose and type of “physical labor” and “lifting”. As that comes up in the literature, I’ll try to keep you posted. Be well, and if you want my personal advice based on clinical experience…hip hinge when you bend towards the floor. If you need help figuring out how to do that hip hinge thingy, go here…

References:

Here are 3 new exercises that subscribers have requested at MyRehab. Full versions of the exercises are available for subscribers to send to their patients to help with patient education. As always, this process is easy to perform and allows you to send these videos directly to your patient’s email in-box. If you’re not yet a subscriber, you can trial MyRehab for 30 days for $1 by signing up here. Monthly membership after that is only $19.99 without contract or obligation. More info is on the video to the right of the page here

1. YTWL-Standing:  Based on Blackburn’s rotator cuff research, this standing version requires fewer props at home using a piece Theraband. The prone version is already in the library at MyRehab.
2. Quadruped Rock Back-Gym Ball:  This is a nice correction for loss of lumbar lordosis at the bottom of squatting exercises. Sometimes referred to as “butt winking”, this rounding of the lumbar spine under load produces the injury vector for lumbar disc herniation.
3. Pallof Presses:  Named after John Pallof, PT, these core stabilization exercises are a great intervention for rotary instability. Standing versions on 2 legs are shown as well as single leg versions. I’ve had a lot of success using the single leg version in runners prone to overpronation and patellofemoral syndrome.

Craig Liebenson, Stuart McGill, Gray Cook

This past weekend I had the pleasure to attend the Stuart McGill – Gray Cook Summit at Stanford University hosted by Dr. Craig Liebenson. I’ve allowed the information to gel for about a week as I considered how what I learned may affect my practice on a day-in and day-out basis. One of the most refreshing takeaways from the weekend was a sense of collaboration between the parties involved. What had all the potential of turning into a contentious weekend with various camps trying to defend their area of expertise, turned into a Kumbaya moment with all involved focused more on how we can combine our resources to help others rather than fighting amongst ourselves. Since I greatly respect both of these individuals and use their approaches in practice daily, I was excited to see that mutual respect on stage and in the break-outs.

Click Here to Get the DVD of the McGill-Cook Summit at Stanford!

A recap of the summit has already been well laid out by Dr. Bobby Maybee, Patrick Ward, Dave Draper and Dan John, so I wanted to focus this post on the clinical gleanings of the weekend. Let’s get solution oriented and try to build a better mousetrap shall we?  I’ll start with the pros of the FMS that all of us in attendance seemed to agree on…

 — allows the trainer or coach to quickly screen a group or team and take painful movements off of the training floor and put them in the clinic prior to training.

 — establishes a numerical rating system and nomenclature that allows better communication between rehab and performance professionals. To my mind, this is somewhat analogous to getting a drivers license and learning to read road signs.

 — helps bring exercise as an intervention into the clinical environment.

— encourages perception of QUALITY of movement and the possible association between poor quality of movement and injury risk.

My personal feeling is that if we stop right there and the FMS never does anything else…then it has provided an invaluable service with those things above. Let’s don’t put it out to pasture quite yet though, huh? Let’s talk about what needs improvement…

Be better.

Common errors by novice users of the FMS were discussed by both Gray Cook and Stuart McGill and they both agreed that these result in problems with the FMS in general. If you’re guilty of these errors, stop! You’re making the FMS look bad!

1. Training decisions based on the summed total of the screen rather than attacking low values and asymmetries.

2. Assuming that the presence of 0’s, 1’s or low summed total score does not mean the client can’t train, you just have to be smart about how you do it. It also means you need to know if you’re smart or not.

3. Many novice users perceive that an adequate score on the FMS is sufficient information to load volume and intensity without further assessment.

These issues represent poor use of a good tool so better education and chats like this can help to improve that, hopefully. Now let’s discuss some of the places where the chassis the FMS is built on might need some work.

Current shortfalls of the FMS were discussed at Stanford and the concerns that came up were…

1. It does not predict injury as well as hoped. Some subgroups it works okay in, but in the general population not so well.

2. It does not account for lumbar hinging, i.e. loss of lumbar lordosis with movement.

3. It still does not account for lumbar hinging. (See what I did there?)

4. A good score on basic movement does not necessarily mean that that movement quality will transfer to daily tasks.

Dr. McGill consistently brought evidence to the table to suggest that if we are to assess injury risk then these specifics need to be accounted for:

1. Understand the biomechanical challenges, loads, and exposure variables associated with a particular task or sport.

2. Understand the available literature associated with the common injuries associated with that specific sport or task.

3. Apply specific coaching techniques to avoid potentially provocative positions, loading strategies, and exposure variables.

He showed studies he’s done (in preparation for press) that show that you can score a 3 on an overhead squat on the FMS and then still show crappy form picking up a coin from the floor and with other daily squatting and lifting movements.

So coaching of movement quality is a good idea that evidence suggests can prevent injury? I like it! So what does that look like? The demo session in the afternoon at the summit provided a glimpse.

A volunteer from the audience, Will Nassif, was 1st screened using FMS on stage by Dr. Kyle Kiesel and Dr. Mark Cheng. Will received a score of 15 with no zeros or ones. Of note, he scored a 3 on the squat test.

Gray Cook oversees FMS-ing of Will Nassif by Drs. Kyle Kiesel and Mark Cheng.

Subsequently, Dr. McGill attempted to demonstrate some of the specific tasks that he recently applied to a firefighter community. One of those tasks included a loaded rope pull, hand-over-hand. In positioning Will in a good neutral spine, braced position, Dr. McGill noted an antalgic positioning in Will’s lower back as he placed his hand on the lumbar spine to palpate his movement quality in that area on set up. At this point he asked will if he had previously had a disc injury. It was revealed that he had and that he had been rehabbing it (BTW, Will gave permission for this public revelation of his status).

Stu McGill demos rope-pull mechanics to Will Nassif while Dr. Craig Liebenson and Dr. Jason Brown look on.

In the set up for the hand-over-hand rope pull, Dr. McGill repeatedly positioned and coached Will through the movement to preserve a neutral spine throughout. As an aside here, I have to take issue with my friend Patrick Ward’s ending note in his excellent recap of the weekend when he stated that McGill’s approach to movement screening is to “put the person under load and see what happens.” From my experience with Dr. McGill over the years, I can say that his history, movement assessment and manual exam are exhaustive. As Stu pointed out, this process takes about 3 hours. Patrick and I chatted about this over pints and agreed that the overall process we observed on stage was what we should all doing in good practice. Do a general movement screen to see if the person can tolerate an unloaded challenge and then observe how the controlled loading affects the system. What Stu took care to do was to assess the integrity of Will’s L-spine position prior to loading.

Dr. Mark Cheng and I take turns being a “load on a rope”.

This pointed out the biggest thing that some of us see as a problem with the current FMS. There is no screen for quality of the movement about the lumbar spine. Some might argue that that info comes out in the hurdle step or the leg raise and I might agree, but when the picture below is presented as a 3 (by definition, movement that is exemplary and can’t be improved on) then some trainer is going to assume that that gives them license to load that back in that position.

I think I hear a train…

That back in that position might get by with that movement for a while but will likely fail in that spinal hinge sooner or later. To my mind, for durability, how you achieve the movement is more important than whether you can perform the movement. Could this gent get to that depth with a lumbar lordosis with corrective exercise? Possibly. But he may also have anatomical limitations that prevent that, like the s0-called “Scottish hip” that Stu has pointed out in the past. At Stanford, he once again brought this up in assessment of a couple of hips, pointing out that sometimes you might just need to avoid ATG squatting due to anatomy. Bottom line, squatting deeply has a point of diminishing returns past the point where you can maintain lordotic curve in the L-spine.

Below you can see what the genes and the training combined will allow in a world champion Oly lifter. My simplest recommendation would be make the 3 for the OH Squat look like Jerzy Gregorek’s below, with a well-preserved L-spine lordosis in the hole. All else is a 2 or less.

Click here to view the embedded video.

• It seems that we need to stop short of using the FMS as a prediction tool for future injury unless further studies define subgroups with which it’s more effective.

• Summed scores don’t offer much info unless below 14, and that might have a ± variance of 2.

• 0’s still warrant referral for clinical eval.

• Don’t assume that a >14 score and no 0’s or 1’s on the FMS gives a green light to load a pattern without further specific assessment. It would be great if I came up with that idea, but Gray actually did in Athletic Body in Balance some time ago.

In closing, special thanks to Craig Liebenson for organizing this party and to Gray and Stu for the time and courage to pull it off and to Laree Draper for archiving it. Now let’s get our there and help some folks!

Find McGill’s and Cook’s Methods Available for Your Clinical Use at MyRehabExercise.com 

We’ve added many new exercises from the FMS Library to the MyRehab Library for our subscribers to use! If you want to see what those look like, a representative channel of full videos from MyRehab is below for a limited time. The rest of the FMS library can be seen by MyRehab subscribers. Those that are not yet savvy to the Functional Movement System (FMS) can learn more at the link here.

To learn more about MyRehab check out the video in the sidebar to the right of the page.

The video channel below will be active until January 31, 2014. If you come here after that and want to see the content on this channel, contact me directly at [email protected] and I’ll give you the password.

Hamstring Strength & Coordination:

• 2 legged gymball curls
• 1 leg gym ball curls

T4 Mobes

• Active Prayer Pose
• Lewit’s Wall Assisted T4 Mobe

Hip Activation/Mobility/Centration

• Clamshell
• Resisted Clamshell
• Reverse Clamshell
• Closed Clamshell

Shoulder/Chest

• Basic Push up with cues for painfree performance

Thoracopelvic Cannister Maintenance

• Wall Bug Progression-Extension Bias
• Wall Bug Progression-Pelvic Lift

 

]]> http://www.myrehabexercise.org/blog/new-dns-inspired-material-on-myrehab/ Mon, 23 Dec 2013 05:40:53 +0000 http://www.myrehabexercise.org/blog/?p=1648 Click here to view the embedded video.

There’s a boatload of new exercises currently on the editing table which will be released to MyRehab subscribers over the next several weeks. Those that have taken some of the DNS coursework will be happy to find supine 3.5 month old to 10 month old Bear Crawl progressions represented. You can view those full videos in the video channel below until January 7, 2014. If you’ve come to this post after that date and want to see what that material looks like, consider a 30 day trial of MyRehab for $1. If you like it, the monthly subscription fee is just $19.99. Keep an eye out for upcoming releases featuring the excellent exercises represented in Evan Osar’s book and from the coursework of running injury researcher Irene Davis. Remember as well that ISCRS members receive 50% discount on their MyRehab subscription! Be well.

 

 

 

]]> http://www.myrehabexercise.org/blog/research-review-check-out-those-hips/ Tue, 28 May 2013 02:12:02 +0000 http://www.myrehabexercise.org/blog/?p=1374

A recent paper from the Mayo Clinic in Rochester, MN (Yuan et al, 2013) appeared in the American Journal of Sports Medicine which brought to light that screening the hip range of motion (ROM) in young athletes might be worthwhile to identify problems that might be in that athlete’s future. Yuan, et al found that a simple modified flexion/adduction/internal rotation (FADIR) impingement test in asymptomatic athletes was able to pick up early stages of cam type of femoracetabular impingement (FAI). Specifically, they assessed 226 athletes for internal rotation deficits by flexing the supine athlete’s hip to 90 degrees, and then applying adduction and internal rotation. They also received the impingement test which was essentially the same test with hip flexion performed to endrange. 19 of those athletes (8%) demonstrated IR <10 degrees and 34 of 38 hips in those athletes demonstrated <10 degrees IR-ROM. Only 18 of those hips had pain with the impingement test. Of those with positive findings, 13 chose to participate in the study. A control group of 13 was chosen from normals from the the original N=226 cohort and both groups received Xray, MRI, and a subsequent manual exam.



Recruitment for Yuan, et al, 2013.

Significant findings included:
• Mean alpha angle on MRI was 44.3 in the control group and 58.1 in the study group.
• 86% of those asymptomatic hips with clinical signs in the study group demonstrated abnormal findings on plain film Xray.
• >2/3 of the study group had MRI demonstrated pathology vs. 1/3 of the study group. The more accurate MRA assessment was not ok’d by IRB for pediatric population.

 

The final paragraph is excerpted below, which asks some important questions we need to answer in future studies:

 

“As more information about the natural history of FAI becomes available, it will be important to understand how and why the pathoanatomy of FAI leads to future hip injuries in some patients. Specifically, if there is a way to easily screen for those with reduced hip clearance, does counseling those patients on avoiding activities that require forced hip motion to the extreme reduce the development of symptomatic FAI or even OA in the future? Currently, we do not recommend any sports-related or activity modification based on the results of a ‘‘positive’’ screening examination result. This study, however, provides new data that can be used to compare future longitudinal natural history studies. Obviously, the data on the natural history of FAI are necessary before definitive recommendations regarding activity modification for the adolescent athlete can be made, such as avoiding ballet or playing as a goalie in hockey.  Additionally, there is probably a little role for prophylactic surgery. However, our findings suggest that a simple hip examination may have utility as a screening test in asymptomatic patients to detect the hip at risk of future pathological changes secondary to impingement during high-risk activities.”
 

 

A few other questions came up for me in my review of this material. I’ve included those questions and links for those that are interested in chasing this out a bit further.

 

1. How do post surgical FAI hips fare in kids, adolescents and adults?-(Philippon 2008, Philippon 2009) Pretty good…if you ask a surgeon.

 

2. What’s the current thinking on most effective clinical exam for the hip? (Martin et al, 2006) A test cluster is suggested but has not yet been thoroughly researched.

 

3.  What are the methods of assessing the alpha angle in the hip?

From Taunton on OrthopedicsOne reference site, on AP Xray or MRI, “the alpha angle is formed by a line drawn from the center of the femoral head through the center of the femoral neck, and a line from the center of the femoral head to the femoral head/neck junction, found by the point by which the femoral neck diverges from a circle drawn around the femoral head.  At present, the upper end of normal is an alpha angle of 50 – 55 degrees.” Serbian researchers (Andjelkovic, 2013) recently described a newer method of radiographically assessing the alpha angle on plain film.

 

4.  What other studies implicate the alpha angle in hip pathology? (Beaule, 2012) Makes one wonder if heavy back squats and ATG cueing in those squats is a good idea in adolescents.

 

5.  If high alpha angle indicates structural predisposition to hip pathology, what exercise and/or rehab can we suggest for our patients?

 

  I really like the combo of DNS-influenced exercise progressions that Jeff Cubos, DC put together on his blog.



In closing, several studies have suggested that in young populations, the presence of FAI in young active patients is likely to lead to significant osteoarthritis in later years.(Ganz, 2003; Tanzer, 2004; Wegner, 2004) In older populations the jury is still out.  Hartofilakidis et al in 2011 performed a retrospective study and tracked 96 asymptomatic, middle-aged hips with radiological evidence of FAI and found “…that a substantial proportion of hips with femoroacetabular impingement may not develop osteoarthritis in the long-term. Accordingly, in the absence of symptoms, prophylactic surgical treatment is not warranted.”

 

References:

Yuan BJ, Bartelt RB, Levy BA, Bond JR, Trousdale RT, Sierra RJ. Decreased Range of Motion Is Associated With Structural Hip Deformity in Asymptomatic Adolescent Athletes. Am J Sports Med. 2013 May 22.

Philippon MJ, Yen YM, Briggs KK, Kuppersmith DA, Maxwell RB. Early outcomes after hip arthroscopy for femoroacetabular impingement in the athletic adolescent patient: a preliminary report. J Pediatr Orthop. 2008 Oct-Nov;28(7):705-10.

Philippon MJ, Briggs KK, Yen YM, Kuppersmith DA. Outcomes following hip arthroscopy for femoroacetabular impingement with associated chondrolabral dysfunction: minimum two-year follow-up. J Bone Joint Surg Br. 2009 Jan;91(1):16-23.

Andjelković Z, Mladenović D. Measuring the osteochondral connection of the femoral head and neck in patients with impingement femoroacetabular by determining the angle of 2alpha in lateral and anteroposterior hip radiographic images. Vojnosanit Pregl. 2013 Mar;70(3):259-66.

Klaue K, Durnin CW, Ganz R. The acetabular rim syndrome. A clinical presentation of dysplasia of the hip. J Bone Joint Surg Br. 1991 May;73(3):423-9.

Martin RL, Enseki KR, Draovitch P, Trapuzzano T, Philippon MJ. Acetabular labral tears of the hip: examination and diagnostic challenges. J Orthop Sports Phys Ther. 2006 Jul;36(7):503-15.

Ganz R, Parvizi J, Beck M, Leunig M, Notzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;417:112-120.

Tanzer M, Noiseux N. Osseous abnormalities and early osteoarthritis: the role of hip impingement. Clin Orthop Relat Res. 2004;429:170- 177

 

Wenger DE, Kendell KR, Miner MR, Trousdale RT. Acetabular labral tears rarely occur in the absence of bony abnormalities. Clin Orthop Relat Res. 2004;426:145-150.

 

Beaulé PE, Hynes K, Parker G, Kemp KA. Can the alpha angle assessment of cam impingement predict acetabular cartilage delamination? Clin Orthop Relat Res. 2012 Dec;470(12):3361-7.

Hartofilakidis G, Bardakos NV, Babis GC, Georgiades G. An examination of the association between different morphotypes of femoroacetabular impingement in asymptomatic subjects and the development of osteoarthritis of the hip. J Bone Joint Surg Br. 2011 May;93(5):580-6.

]]> http://www.myrehabexercise.org/blog/help-promote-myrehab-in-your-presentation/ Sat, 06 Apr 2013 23:07:16 +0000 http://www.myrehabexercise.org/blog/?p=1316 If you are a public speaker who presents to groups and are a subscriber or advocate for MyRehabExercise.com, you can help us get the word out by including the slide below in your presentation. Click here to link to larger version PDF with better resolution and drag it right into your Powerpoint or Keynote presentation. Thanks for your help getting the word out!!



 

 

 

 

 

 

 

 

 

 

 

Also, the International Society of Clinical Rehabilitation Specialists (ISCRS) is a multidisciplinary group of healthcare pros dedicated to sharing and promoting the emerging rehab and performance methodology with each other and with the general public. Members of ISCRS enjoy a 50% discount to MyRehabExercise.com and similar discount to other incredibly informative sites like SportsRehabExpert.com and StrengthCoach.com. Check it out!

 

 

 

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