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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)
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.
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.
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:Haro H, Crawford HC, Fingleton B, MacDougall JR, Shinomiya K, Spengler DM, Matrisian LM. Matrix metalloproteinase-3-dependent generation of a macrophage chemoattractant in a model of herniated disc resorption. J Clin Invest. 2000 Jan;105(2):133-41. Jacobs WC, van Tulder M, Arts M, Rubinstein SM, van Middelkoop M, Ostelo R, Verhagen A, Koes B, Peul WC. Surgery versus conservative management of sciatica due to a lumbar herniated disc: a systematic review. Eur Spine J. 2011 Apr;20(4):513-22. Henmi T, Sairyo K, Nakano S, Kanematsu Y, Kajikawa T, Katoh S, Goel VK. Natural history of extruded lumbar intervertebral disc herniation. J Med Invest. 2002 Feb;49(1-2):40-3. Saal JA, Saal JS, Herzog RJ : The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 15 : 683 – 686, 1991. Bozzao A, Gallucci M, Masciocchi C, Aprile I, Barile A, Passariello R : Lumbar disc herniation. MR imaging assessment of natural history in patients treated without surgery. Radiology 185 : 135 – 141, 1992. Delauche – Cavaillier MC, Budet C, Laredo JD, Debie B, Wybier M, Dorfmann H, Ballner I : Lumbar disc herniation. Computed tomography scan changes after conservative treatment of nerve root compression. Spine 17 : 927-933, 1992. Komori H, Shinomiya K, Nakai O, Yamaura I, Takeda S, Furuya K : The natural history of herniated nucleus pulposus with radiculopathy. Spine 21 : 225 – 229, 1996. Teplic JG, Haskin ME : Spontaneous regression of herniated nucleus pulposus. AJNR 6 : 331- 335, 1985. Yukawa Y, Kato F, Matsubara Y, Kajino G, Nakamura S, Nitta H : Serial magnetic resonance imaging follow-up study of lumbar disc herniation conservatively treated for average 30 months. Relation between reduction of herniation and degeneration of disc. J Spinal Disord 9 : 251- 256, 1996. Orief T, Orz Y, Attia W, Almusrea K. Spontaneous resorption of sequestrated intervertebral disc herniation. World Neurosurg. 2012 Jan;77(1):146-52. Iwabuchi M, Murakami K, Ara F, Otani K, Kikuchi S. The predictive factors for the resorption of a lumbar disc herniation on plain MRI. Fukushima J Med Sci. 2010 Dec;56(2):91-7. Reyentovich A, Abdu WA. Multiple independent, sequential, and spontaneously resolving lumbar intervertebral disc herniations: a case report. Spine (Phila Pa 1976). 2002 Mar 1;27(5):549-53. Cribb GL, Jaffray DC, Cassar-Pullicino VN. Observations on the natural history of massive lumbar disc herniation. J Bone Joint Surg Br. 2007 Jun;89(6):782-4. Zhou G, Dai L, Jiang X, Ma Z, Ping J, Li J, Li X. Effects of human midkine on spontaneous resorption of herniated intervertebral discs. Int Orthop. 2010 Feb;34(1):103-8. doi: 10.1007/s00264-009-0740-2. Epub 2009 Mar 11. Doita M, Kanatani T, Ozaki T, Matsui N, Kurosaka M, Yoshiya S. Influence of macrophage infiltration of herniated disc tissue on the production of matrix metalloproteinases leading to disc resorption. Spine (Phila Pa 1976). 2001 Jul 15;26(14):1522-7. ItoT,YamadaM,IkutaF,etal.Histologic evidence of absorption of sequestration-type herniated disc. Spine 1996;21:230–4. Fagerlund MK, Thelander U, Friberg S. Size of lumbar disc hernias measured using computed tomography and related to sciatic symptoms. Acta Radiol 1990;31(6):555–8. Maigne JY, Rime B, Deligne B. Computed tomographic follow-up study of forty-eight cases of nonoperatively treated lumbar intervertebral disc herniation. Spine (Phila Pa 1976) 1992;17(9):1071–4. Bush K, Cowan N, Katz DE, et al. The natural history of sciatica associated with disc pathology. A prospective study with clinical and independent radiologic follow-up. Spine (Phila Pa 1976) 1992; 17(10):1205–12. Jensen TS, Albert HB, Soerensen JS, et al. Natural course of disc morphology in patients with sciatica: an MRI study using a standardized qualitative classification system. Spine (Phila Pa 1976) 2006;31(14): 1605–12 [discussion: 1613]. Autio RA, Karppinen J, Niinimaki J, et al. Determinants of spontaneous resorption of intervertebral disc herniations. Spine (Phila Pa 1976) 2006; 31(11):1247–52. Monument MJ, Salo PT. Spontaneous regression of a lumbar disk herniation. CMAJ 2011;183(7):823. David G, Ciurea AV, Mitrica M, Mohan A. Impact of changes in extracellular matrix in the lumbar degenerative disc. J Med Life. 2011 Aug 15;4(3):269-74. Tsarouhas A, Soufla G, Katonis P, Pasku D, Vakis A, Spandidos DA. Transcript levels of major MMPs and ADAMTS-4 in relation to the clinicopathological profile of patients with lumbar disc herniation. Eur Spine J. 2011 May;20(5):781-90 Adams MA, Hutton WC. Prolapsed intervertebral disc. A hyperflexion injury 1981 Volvo Award in Basic Science. Spine (Phila Pa 1976). 1982 May-Jun;7(3):184-91. Vo NV, Hartman RA, Yurube T, Jacobs LJ, Sowa GA, Kang JD. Expression and regulation of metalloproteinases and their inhibitors in intervertebral disc aging and degeneration. Spine J. 2013 Mar;13(3):331-41. Zigouris A, Batistatou A, Alexiou GA, Pachatouridis D, Mihos E, Drosos D, Fotakopoulos G, Doukas M, Voulgaris S, Kyritsis AP. Correlation of matrix metalloproteinases-1 and -3 with patient age and grade of lumbar disc herniation. J Neurosurg Spine. 2011 Feb;14(2):268-72. Weiler C, Nerlich AG, Zipperer J, Bachmeier BE, Boos N. 2002 SSE Award Competition in Basic Science: expression of major matrix metalloproteinases is associated with intervertebral disc degradation and resorption. Eur Spine J. 2002 Aug;11(4):308-20. Bachmeier BE, Nerlich A, Mittermaier N, Weiler C, Lumenta C, Wuertz K, Boos N. Matrix metalloproteinase expression levels suggest distinct enzyme roles during lumbar disc herniation and degeneration. Eur Spine J. 2009 Nov;18(11):1573-86. Guterl CC, See EY, Blanquer SB, Pandit A, Ferguson SJ, Benneker LM, Grijpma DW, Sakai D, Eglin D, Alini M, Iatridis JC, Grad S. Challenges and strategies in the repair of ruptured annulus fibrosus. Eur Cell Mater. 2013 Jan 2;25:1-21. Review. Peng BG. Pathophysiology, diagnosis, and treatment of discogenic low back pain. World J Orthop. 2013 Apr 18;4(2):42-52.
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
- 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.
- 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.
- 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.
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.
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…
— 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.
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…
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.
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).
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.
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.
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.
So what are we left with from the weekend? The way I see it:
- 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!
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.Significant findings included:
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:
- 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.
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.Tanzer M, Noiseux N. Osseous abnormalities and early osteoarthritis: the role of hip impingement. Clin Orthop Relat Res. 2004;429:170- 177Wenger 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.
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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!
Elbow Treatment 1.0
Lateral elbow pain (lateral epicondylitis, AKA tennis elbow, radial nerve entrapment syndromes) is a frequent presentation in our clinic March-May as folks who started a weight routine for a New Year’s resolution begin to ‘crash and burn’ as poor form leads to tissue failure in the extensor tendons for the wrist. Nirschl described a surgical technique in the 1970s which was highly effective at relieving this condition. Common current wisdom is that the putative cause of pain is related to the commonly observed granulation tissue associated with the ‘mobile wad of 3’ extensor tendons. Co-morbidity we frequently see in clinic may include entrapment neuropathies and Miller and Reinus, in 2010 provided a nice review of those. While this is interesting from a structural perspective and helps to inform manual therapies addressing this condition, it is not the thrust of this article. Let’s examine lateral elbow pain from a functional point of view.
Elbow Treatment 2.0
Borrowing a page from the Joint by Joint approach, the elbow is a hinge joint somewhat analogous to the knee. The literature suggests that many of the maladies of the knee can be addressed by working on strength and mobility around the hip. Similarly with the elbow, we see a stable joint complex surrounded by comparatively more mobile shoulder and wrist joints. Consistent with Joint by Joint, poor mobility in the inherently mobile joint structures will lead to the body “asking for” more mobility in a stable joint complex, in this case the elbow. Often using this approach and working through shoulder mobility and stability we can have a great impact on the long-term function of the elbow. In the last several years this approach has been quite useful in reducing treatment time and improving outcomes in this condition in our clinic. Typically we would focus on improving scapular mobility often using Stecco’s manual therapies to assure appropriate scapular retraction and protraction. Upper thoracic joint mobilization or manipulation was also quite helpful in improving overall shoulder mechanics by improving mobility in the scapular thoracic articulation and in the thoracic spine in order to spare the glenohumeral articulation. A patient in our clinic today provided an excellent example of an even more modern approach integrating DNS principles with the joint by joint and manual therapy methodology.
Elbow Treatment 3.0
SR, a 35-year-old public safety officer, presented with left lateral elbow pain which began insidiously over the past several weeks. Eight weeks before he had started a self-improvement project involving weightlifting using a four day split. Prior to that it had been several years since he had engaged in regular weightlifting. Significant prior history included several incidents of shoulder injury and near dislocations on the affected side. Painful ADLs included reaching for the milk in the back of the refrigerator, lifting a coffee cup, opening a heavy door or gripping the handlebars of his mountain bike. In the gym, patient found benchpress, and overhead pushing and pulling exercises to be provocative.
In standing, left arm was inwardly rotated and the humerus was palpated in an anteriorly displaced position in the glenoid. Shoulder abduction, external rotation and extension were painlessly limited in active range of motion. Palpation over the left lateral epicondyle of the humerus, passive left wrist flexion, resisted left wrist extension, and strong handshake all produced pain at CC. Strong handshake produced 6/10 severe pain. Intra-abdominal pressure (IAP) assessment revealed rib flare, apical breathing pattern and poor ability to pressurize the thoraco-pelvic canister. Spinal segmental extension restrictions were noted in the thoracic spine. ULNNTs were negative and Spurling’s suggested no radicular involvement.
A structural diagnosis of lateral epicondylitis was rendered with functional contributors including:
- poor IAP/respiratory pattern per DNS protocols,
- poor shoulder mobility leading to overuse of the stability-loving joint complex per Joint by Joint approach.
We decided to begin with DNS-informed protocols first to see if patient would be able to correct most of his own condition utilizing functional corrective exercise. We decided that afterward we would address joint and myofascial components as deemed necessary.
Patient was instructed in diaphragmatic breathing while maintaining rib tuck position and long spine. That pattern formed the basis for all subsequent exercises. We then trialed dead bug, wall bug and foam roll progressions and the latter 2 were within patient’s functional pain free range. In short as Dr. Craig Liebenson would put it, they were the most difficult exercises the patient could perform excellently. To see Dr. Liebenson apply this approach you can check out this video. To assist with thoracic extension while providing a closed chain weight-bearing position for the affected joint complexes patient was coached in modified Sphinx exercise. Before manual therapy was applied, a mid-treatment audit was performed as a handshake test. With firm grip patient smiled widely and noted that he only had 1/10 severe pain in the lateral elbow. Objectively, the strength of the grip was quite a bit more robust.
Subscribers to MyRehabExercise.com may view the above videos by clicking on the images.
Manual therapy included prone manipulation of the T4 segment into extension as well as prone combo manipulations of the upper ribs. Glenohumeral rotation mobilizations were provided in internal and external vectors through abduction and flexion ranges of motion to aid in joint capsule mobility. Graston technique was provided using gua sha type rapid stroke movements proximal to distal to improve blood flow and oxygenation of the extensor muscles. This concluded the treatment portion of the first encounter. Total amount of contact time for this established patient with new presentation was 30 minutes. A posttreatment audit was performed as strong handshake and patient had 0/10 severe pain in the lateral elbow and his grip strength was markedly improved. He received emailed exercise prescription follow-up of all of these exercises from MyRehabExercise.com. He was scheduled for a return visit in one week which will likely consist of manual therapies per Stecco protocols to improve scapulothoracic mobility and joint centration of the glenohumeral articulation. typical follow-up exercise at that time will likely be closed chain DNS exercises such as Tripod Sit and Bear Crawling and Therabar Eccentrics.
Previous blog posts here outlined the rationale for addressing the deep spine stabilization system and respiratory pattern in this case. Below is the graphic that shows how those dominoes stack up.
According to DNS theory, the hypertonic upper trapezius represents an adaptational motor program for shoulder stabilization. In the absence of an adequate punctum fixum with a well functioning deep spine stabilization system, lower trapezius and serratus anterior are unable to stabilize the scapula against the chest wall. The upper trapezius is then placed into a primary role to stabilize the shoulder girdle by “plugging it in” to the cervicothoracic area. The resultant alteration in biomechanics pitches scapula upwards and forwards in the shortening of the pectoralis minor and internal rotators. The hypertonicty in these muscles in turn de-centrates the humeral head in the glenoid. While the clinician and manual therapist can positively impact the course of care with manual method alone, adding this kind of foundational corrective exercise dramatically decreases the treatment time and improves the overall musculoskeletal health of the patient. Much of this exercise work can also be provided by a heads up personal trainer who has learned these techniques, but the trainer should have a DC or PT help on the pain management end. Better yet, those trainers who are familiar with DNS assessment techniques for their work, can help avoid having their clients on the disabled list where they can’t train at all.
I will try to follow up with this patient on the blog in future posts. In the meantime, consider MyRehabExercise.com for excellent patient/client oriented videos for the correctives shown above as well as many more to help with your functional exercise instruction. Click on the link below to learn more!
Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. J Bone Joint Surg Am. 1979 Sep;61(6A):832-9. PubMed PMID: 479229.
Miller TT, Reinus WR. Nerve entrapment syndromes of the elbow, forearm, and wrist. AJR Am J Roentgenol. 2010 Sep;195(3):585-94. doi: 10.2214/AJR.10.4817. Review. PubMed PMID: 20729434.
Powers CM. The influence of abnormal hip mechanics on knee injury: a biomechanical perspective. J Orthop Sports Phys Ther. 2010 Feb;40(2):42-51. doi: 10.2519/jospt.2010.3337. Review. PubMed PMID: 20118526.
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):230-6. PubMed PMID: 20140154; PubMed Central PMCID: PMC2813499.
In recent conversations with students in my office and with colleagues curious to learn more about how Dynamic Neuromuscular Stabilization (DNS) works “on the ground” in practice, I have attempted to bring together an overview that can be readily understood for these folks. Full disclosure…at this point (2-17-2013) I have completed DNS training through the “C” level of clinical practice and “Sport” courses 1 &2. This level of training does not qualify me to be an instructor in the DNS system, so all of my musings here should be taken with a grain of salt and are trumped by those who have received those more advanced qualifications. Therefore, think of this post as my own personal musings as I attempt to integrate the work into my sports-injury/rehab-focused practice of chiropractic and take what you will from it. The graphic below was my attempt to explain the flow of common musculoskeletal injury and dysfunction through the DNS lens. Below that, we’ll examine each of these points so that we can see how this pattern recurs with our patients. In future posts, we may refer back to this post to help frame specific Case Studies.
1. Apical Respiration-When Stress Somatisizes
One of the primary tenets of DNS is the importance of breathing stereotype. The effects of inefficient respiration carry over to other disciplines of health care such as cardiology (1,2,3), gastroenterology (4), pain management (5) and psychology (6) as well. In the DNS model, breathing patterns that are high in the chest, rapid and shallow (apical) can result in altered position of the diaphragm. (7)
2. Disruption of Native Spine Stabilization Strategies
Using the muscles of the ‘deep core’ (multifidii, transversus abdominis, pelvic floor and diaphragm), spine stabilization can occur via improved intra-abdominal pressurization. (8,9) This video by Gray Cook, PT speaks to this topic from a tangential viewpoint.
3. Adaptation of High Threshold Stabilization Strategies
When optimum stabilization strategies are not available, phasic muscles typically used for prime movement are used to both move and to provide alternate stabilization strategies. These strategies for movement often result in joint de-centration which leads to less-than-optimal performance. If loads are too high, too intense, or too frequent joint degeneration and tissue failure may be the result. Charlie Weingroff, DPT speaks to this below.
4. Structural Adaptations of Myofascial Elements
Langevin and other researchers have shown that the fascial remodeling occurs in those with chronic low back pain (CLBP) and that the lumbodorsal fascia of those with CLBP is 25% thicker than in controls. (10,11) The presence of ‘tunnel syndromes’ involving superficial neurology has been well described. (12) Janda’s Crossed Syndromes spoke to inhibition of agonists in the presence of shortening of antagonists. This pattern was later updated by Gray Cook and Mike Boyle and is now referred to as the Joint by Joint Approach. As synergistic muscles are re-tasked to shoulder the load left by inhibited muscles, remodeling of the muscle can change its texture, pliability and result in fascial remodeling in the involved muscles. This may also result in superficial entrapment of local superficial nerves and result in local neuralgia in the absence of joint or muscle injury. This point in the process is where manual therapy has the most direct impact and allows bodyworkers an in-road on understanding and treating patients using a functional approach.
5. Tissue Failure/Degeneration and Diminished Performance
Langevin also theorized in her paper on thoracolumbar fascia,
“Possible explanations for reduced thoracolumbar fascia shear strain during passive trunk flexion in LBP include abnormal patterns of trunk muscle activity and/or intrinsic connective tissue pathology.” (13)
In the DNS model, we may see common injuries develop around the hip, knee, shoulder and elbow in response to the aberrant loading of those joints in these scenarios. Rather than structure-focused treatments to address the site of pain, practitioners assess movement and stabilization strategies and address those non-painful dysfunctions to effect long lasting beneficial changes. Similarly, in the FMS model, we screen for asymmetrical movement patterns and correct the non-painful dysfunction. These last 2 areas we will save for further explorations with case studies to demonstrate the clinical applications of the combined structural-functional methods. We will also show those corrective exercise interventions featured on MyRehabExercise.com.
- Anderson DE, et al. Regular slow-breathing exercise effects on blood pressure and breathing patterns at rest. Journal of Human Hypertension. In press. Accessed Nov. 9, 2010.
- Gavish B. Device-guided breathing in the home setting: Technology, performance and clinical outcomes. Biological Psychology. 2010;84:150.
- Schein MH, et al. Treating hypertension in type II diabetic patients with device-guided breathing: A randomized controlled trial. Journal of Human Hypertension. 2009;23:325.
- Bryan T. Green, MD; William A. Broughton, MD; J. Barry O’Connor, MD, MS(Epid). Marked Improvement in Nocturnal Gastroesophageal Reflux in a Large Cohort of Patients With Obstructive Sleep Apnea Treated With Continuous Positive Airway Pressure. Arch Intern Med. 2003;163(1):41-45. doi:10.1001/archinte.163.1.41.
- Busch V, Magerl W, Kern U, Haas J, Hajak G, Eichhammer P. The effect of deep and slow breathing on pain perception, autonomic activity, and mood processing–an experimental study. Pain Med. 2012 Feb;13(2):215-28.
- Alicia E. Meuret, David Rosenfield, Anke Seidel, Lavanya Bhaskara, and Stefan G. Hofmann. Respiratory and Cognitive Mediators of Treatment Change in Panic Disorder: Evidence for Intervention Specificity. J Consult Clin Psychol. 2010 October ; 78(5): 691–704.
- Kolar P, Sulc J, Kyncl M, Sanda J, Cakrt O, Andel R, Kumagai K, Kobesova A. Postural function of the diaphragm in persons with and without chronic low back pain. J Orthop Sports Phys Ther 2012;42(4):352-362.
- Hodges PW, Eriksson AE, Shirley D, Gandevia SC. Intra-abdominal pressure increases stiffness of the lumbar spine. J Biomech. 2005;38:1873-1880.
- Hodges PW, Cresswell AG, Daggfeldt K, Thor- stensson A. In vivo measurement of the effect of intra-abdominal pressure on the human spine. J Biomech. 2001;34:347-353.
- Langevin HM, Sherman KJ. Pathophysiological model for chronic low back pain integrating connective tissue and nervous system mechanisms. Med Hypotheses 2007;68(1):74–80.
- Langevin HM, Stevens-Tuttle D, Fox JR, Badger GJ, Bouffard NA, Krag MH, Wu J, Henry SM. Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain. BMC Musculoskelet Disord. 2009 Dec 3;10:151.
- Pecina MM, Krmpotic-Nemanic J, Markiewitz AD. Tunnel Syndromes: Peripheral Nerve Compression Syndromes. CRC Press, 2001.
- Langevin et al. Reduced thoracolumbar fascia shear strain in human chronic low back pain. BMC Musculoskeletal Disorders 2011, 12:203
On Jan 10-13 I had the pleasure of attending the DNS-Sport 1&2 courses in LA at Chris Powers’ Movement Performance Institute and given that many have contacted me about the content of the course, thought I should put together a review. My exposure to DNS to date has been through the clinical track of DNS A,B and C certifications (C cert pending) over the past 3 years and may continue with D level in the next year.
I will say that I entered this Sport course with some reticence as I was not sure whether adding more DNS material in my toolbox was going to help much. The primary tools I was looking for, corrective exercises to share with patients, seemed to be an afterthought in my previous courses. My specific points that I was personally concerned about with my prior DNS classes were:
- Too much focus on internal cueing strategies vs external cueing strategies
- Too little focus on corrective exercises to share with patients to reduce need for care
- Prevalence of so-called Vojta ‘reflex stimulation points’ in the course matter
- Poor organization of material and course notes
- Too much focus on pediatrics
So How Were the DNS “Sport” Courses Different?
I was stoked to find that the “Sport” courses had left out pediatrics, reflex locomotion material and internal cueing focus had been de-emphasized! Finally too, exercise strategies we can share with our patients and clients were the focus! I was very excited about this turn of direction in the DNS course work but heard from some of my strength and conditioning (S&C) colleagues that they were concerned about the persistent clinical focus of the course and the hands-on cueing demonstrated. Grand Rounds focused on injured athletes, but instructor Petra Valouchova studiously avoided rendering a diagnosis or focusing on tissue injury. Instead the focus was on movement assessment and correction, these are tenets that are the bailiwick of both the S&C world and in the clinical rehab world thanks to the FMS/SFMA paradigm shift provided by Gray Cook. Statutes and scope of practice restrictions in much of the world prevent trainers and S&C folks from manual contact with their clients, but the roughly 50% population of S&C folks in the room, they saw that this material was easily verbalized to potential clients.
When I came back home to Portland, the only regret I had was that the incredible group of S&C folks that I share patients and clients with did not yet have this material under their belts. While the FMS/SFMA palette gives clinicians and trainers a common language to speak and hand off to each other with, the DNS material has not reached that level of common usage yet. The courses I attended provide that common map from which we can use our respective fields of experience to orienteer.
What’s in a Name?
I think that perhaps the “Sport” designation was a misnomer that grew out of earlier conversations about how to create a template that clinicians and trainers can work from together. I propose that these “Sport” courses are a MUCH better introduction to motor pattern ontogeny and to achievement of proper joint centration to set the stage for performance than are the clinical A, B, C, D level courses. As a result, I think the current Sport courses should carry a name that better reflects their content…something like
- DNS 1-Introduction of Developmental Motor Patterns,
- DNS 2-Application of Functional Joint Centration to Reduce Injury.
- The true “Sport” course, which has yet to be developed, would focus on use of these principles to bring optimal performance to athletics. I’m thinking of a name like DNS 3-Optimizing Performance with DNS Principles. Those venues would be in gyms and weightrooms and Grand Rounds would not be injured athletes, but would instead feature promising athletes at different developmental levels who want to run faster, jump higher, throw farther. I could see those courses using items like Omegawave over subsequent days and OptiGait and slow motion video capture to see pre and post DNS interventions in the healthy athlete. Further coursework could focus on sport specifics…Track and field, Cycling, Tennis, etc. See..now I’m excited!
DNS Sport At Present
For now, the course content of the DNS-Sport classes is as follow:
DNS Sport 1 and 2 are an introduction to ontogenic motor patterns.
Course 1-Focuses on development of deep spine stabilization system via diaphragm/pelvic floor and TA
Course 2-Focuses on joint centration of limbs on the deep spine stabe system. Course 2 also teaches assessment and correction of common motor pattern faults that can lead to injury. Here I’m talking about the chronically tight hip flexors and traps that defy daily stretching techniques. We all see these in clinical practice and might even know them as Upper Cross and Lower Cross through the Janda perspective. However, many of us with manual toolboxes ‘face palm’ daily about the recurrent tightness in those muscles that doesn’t respond to stretching, ART, Graston, foam rolling, lacrosse balls, etc. DNS offers a window to effectively treating these hypertonic muscles by improving intrinsic spine stabilization to take to adaptive stabilization roles these types of muscles off of the table. Phasic muscles return to their movement roles and very quickly decrease hypertonicity when the stabe system is returned.
So, should you, as a trainer or clinician, cough up the $$ to bring this understanding to your patient/client population? IMHO, the answer is an enthusiastic YES!!! Moreover, I think the current DNS-Sport 1&2 courses embody best way to gain access to this material in an organized, well-presented manner…even if the courses are named wrong 😉 In the future, that Performance course I wished for above , will be presented and you will want to have the understanding represented in the current Sport courses. If you want opinions of others that attended the Sport courses, check out the videos below.
Finally for my colleagues in Prague, I would also offer constructive criticism that the courses would be improved by offering a repository of videos to course attendees which offer review of the movement patterns. Perhaps the excellent library that Mike Rintala, DC and Dave Sabo are cranking out can be used! I can imagine a password protected site where attendees could see instructors demonstrating and covering the essential points of prone and supine movements on video for their own review. I could also see benefit in another service for attendees consisting of PDFs of specific exercises that are covered in these courses. These PDFs could contain photos and key points and work as handouts to help the patients and clients do their home exercises. Just a thought!