Case for the Turkish Get Up in Rehab

As rehab professionals we are all well aware at how many (most) individuals, especially those in pain/ chronic pain, lose the ability to perform movement patterns that toddlers so easily perform.  Watching the movements of a toddler will show efficient and seamless  positional transitions including to and from prone, supine, quadruped, half-kneeling, reaching, and effortless full squatting.  These motor patterns remain ingrained in the adult motor-sensory brain maps but they are often shrouded in movement dysfunction as years of motor-sensory neglect compounded on top of concomitant structural changes.  This is why when you try to have the average activity-naive adult perform a full squat it often looks terribly awkward, a far cry from the aesthetic perfection of the toddler squat.  Had the individual continued to reinforce and practice the motor-sensory pathways for their squat during the time periods of structural change their patterns would have adapted to allow for efficient squat despite bodily changes.  As a physical therapist one of my favorite treatments for poor movers and those in pain is to expose them to developmental positions and movement strategies.  For reteaching proper trunk and upper extremity integration I use the Turkish get up exercise, or at least a partial variation of it.  The full Turkish get up can be thought of as the most efficient way to stand up with a weight held overhead in one hand.  There are several small idiosyncrasies in the form used but generally the full movement is observed as in the video below.

So what is going on at the beginning of the movement that I like is the shoulder flexion, linked to scapular protraction, linked to contralateral thoracic rotation.  This is the perfect set up for practicing reach and upper extremity/ trunk integration in a developmental position.  Think of a baby on its back with some object in front of him, just out of reach.  The most efficient way for that baby to try to reach that object is the initial portion of the Turkish get-up, that is shoulder flexion, scapular protraction, and contralateral thoracic rotation.  For rehab purposes, I tend to have patients end the movement when they are in the pseudo-oblique sitting position with arm overhead and weight through the contralateral elbow.  Give it a try!

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Why is treating tendinopathy so tricky?

 

Tendinopathy is an exceedingly common musculoskeletal condition among active individuals.  Tendinopathy has been an increasingly studied topic of sports medicine and rehab with research actually creating more divergence in the pathophysiological mechanisms with the term “tendinopathy” itself leading insight into this history of equivocation.  Painful tendon conditions were termed “tendonitis” pre-1990s then shifting to “tendinopathy” and even “tendinosis” in light of histological studies demonstrating lack of inflammatory cells in chronic, pathological tendons.  However, advances in histological techniques have recently shown that inflammation likely does play some role in the early stages of tendinopathy while it remains generally accepted that later stage, chronic, degenerative tendinopathies are devoid of these inflammatory markers, but this is a growing topic of debate.  In light of the pathology explanation fluctuations, it is without wonder that rehabbing tendinopathy remains difficult.  Treatment options for those treating painful tendons exist with varying degrees of evidence.

Many models and theories of tendon pathophysiology exist.  The most prevalent and accepted theories are those of mechanical overload resulting in a condition of eventual disrepair and disorganization of the tendon.  These could entail possible minor fibril rupture which leads to acute fibroblast proliferation and release of factors surrounding an initial attempt of healing.  This is proposed to lead to neovascularization, the in-growth of blood vessels and nerves, when this healing process does not, for some reason, complete.  We can see these individual steps, such as the common observation of neovascular in-growth, however the actual initial step of partial rupture has not been observed with no evidence demonstrating they actually occur.  Furthermore, in most cases tendinopathies arise symptomatically in a sort of gradual manner without a clear injurious incident, which would be expected with partial rupture.  Biochemical and histological studies have also shown major differences between complete rupture and healing tendons compared to those with tendinopathy with ruptured tendons lacking the presence of common tendinopathic findings suggesting that tendon rupture/failure may not be linked to pre-existing tendinopathy.

There does appear to an acute stimulus triggering tendinopathy with new research now accumulating suggesting inflammation does, in fact, play a role in the early stages of tendinopathy and possibly in the continual progression of the condition.  Some researchers, such as Jill Cook’s group at La Trobe University, assert that this is likely more of a cellular activation than an actually inflammatory response.  This cell activation idea has lead to attempts at staging tendinopathy with the acute and painful tendon being described as the reactive stage whereby mechanical overload triggers cellular activation leading to increases in proteoglycan production.  Increased hydration of these proteoglycans are then said to increase tendon swelling prompting the disruption of collagen alignment and creating areas corresponding to hypoechoic areas prone to neovacularization.  Tendinopathy is proposed by Cook to occur in stages of reactive tendinopathy, tendon dysrepair, and finally tendon degeneration.

Another hypothesis is a sort of pain-first mechanism with the onset of tendon pain representing a change in nociception via primary ingrowth of nerves and vessels.  We do know that eventual nerve and vessel in-growth is present in late stage tendinopathy but it is difficult to determine when this occurs and the directional relationship towards tendinopathy-does tendinopathy result from this neovascular ingrowth or because of it.  It’s plausible that increases in tendon nociception could lead to mechanical offloading both with movement offloading and offloading at the tissue level.  Offloading at the level of tissue itself is an idea termed tendon stress-shielding which is another hypothesis of tendinopathy supported by evidence that chronically unloaded tendons undergo degenerative processes.

Another plausible hypothesis is that mechanical overload could exceed a sort of tendon homeostasis whereby cells responsible for tissue support and regeneration to continual tissue turnover become stressed beyond their capacity to heal the tendon.  This then may even lead to cellular apoptosis at the tendon which has been observed in large increases of load. It has also been suggested that perhaps there is an oxidative stress component in areas of the tendon which become hypoxic under inadequate oxygen supply and have help explain the mechanism of neovascularization observed in chronic tendinopathy.   Clearly other variables could be involved such as genetics and individual factors with such things as high cholesterol and adiposity being correlated with incidence of tendinopathy.

Compression of the tendon at areas of contact with bone also likely play a role especially with insertional tendinopathies whereby muscle contraction causes increased tendon compression into bone perpendicular to the length of the tendon.  A clear example is of the rotator cuff tendons which must bend or wrap around the head of the humerus at their distal attachments.  Muscle activation would cause the tendon to be firmly pressed into the bone as a sort of bow-stringing effect.  In fact, most tendinopathies are likely insertional with the exception being mid-substance achilles tendinopathy.

Adding to the nearly enigmatic pathophysiology  there also is not clear consensus regarding clinical diagnostic criteria for tendinopathy.  Typically,.tendinopathy is generally diagnosed clinically via local pain related to isometric load and tenderness to palpation.  These criteria are said by Mascia to be anecdotal and lacking specificity Furthermore, imagining modalities are typically unavailable to the rehab specialist with imaging results not consistently correlating to clinical presentation (Masci, 2016.)  Pain does not appear to correlate well to the degree of neovacularization and it is known that asymptomatic athletes can undergo pathological degeneration in the absence of pain.  As such it can be difficult to determine the degree of progression of the condition when a patient presents with tendon pain – is this apparent reactive tendon occurring in a recently otherwise healthy tendon, or was there significant degeneration that has now become symptomatic?   So while it is difficult to diagnose and define tendinopathies it does appear that tendons can undergo normalization over a extended periods of time to improvements in tissue structure as observed with ultrasonography.  So how do we, as clinicians, go about treating and rehabbing painful tendon conditions?

There are several proposed therapies for tendinopathy including plasma-rich platelet injection, high volume injection, extra-corporeal shockwave therapy, stem cell therapy, and of course loading therapies.  The best current evidence in treating tendinopathy is that of tendon loading through exercise.  This is an interesting paradox as it is typically accepted that tendon overload and lack of adaptation to load demands to be a primary driver of tendinopathy.  However, research in the area of loading initiated by Hakan Alfredson and others have shown clear benefit to progressive loading.  An unloaded tendon will regress in it’s load capacity and become prone to increased pathology.  This unloading as noted by possible tissue shielding and/or changes in movement patterns are ways a person may instinctively avoid pain by unloading, but could contribute to continued tendinopathic processes as a result.  Tendon loading provides benefits through the mechanisms of mechanotransduction whereby cells respond to physical load with biophysical and biochemical adaptation.  These adaptations occur as results of tenocyte response with changing cellular structure and composition via alteration in gene expression and protein synthesis.  It also appears that load by muscle contraction is better than stretching for maintaining and promoting load capacity in tendons, although some research exists suggesting static stretching may promote improved tendon efficiency/energy preservation as noted with decreased hysteresis (energy loss) when tendons release their stored energy from load after a stretching program (Kubo, 2002.)  In terms of muscle contraction there is more evidence, at present, for eccentric contraction providing benefit, however, evidence of benefit from concentric contraction exist as well just not in as robust of number as those supporting eccentrics.

The paradox of treating a tendinopathic tendon caused by overload with load makes clinical decisions challenging and there does not appear to be any clear consensus advice on the topic.  I tend to favor Jill Cook’s perspective of the acute pain of tendinopathy as a sort of reactive state which should be allowed to subside before controlled loading is initiated.  My general method for treating tendinopathy (which is ever-evolving) is to reverse titrate any clear offending stimulus or activity with some preservation of of tendon loading with pain-free exercise such as isometrics in positions favoring as little tendon compression as possible.  As an example, isometrics for insertional achilles tendonopathy would be avoided initially  in dorsiflexed positioning as it has been proposed this position could promote insertional compression.  When the pain has shown evidence of regression, typically after about a week, I introduce a gradual loading program.  Research at this point indicates that pain is likely to occur but should not be debilitating, such as to the point of making ambulation difficult; pain is expected, but must be endured to an extent during exercise.

Medical intervention show only tenuous benfefit with anti-inflammatory strategies, such as glucocorticoids and NSAIDs, showing inconsistent benefits but mostly in the short, initial time-frame.  Furthermore, longer duration use, or use after the initial reactive stage, may be harmful as we know that longer durations of glucocorticoids decrease tendon quality and NSAIDs impede healing of muscle and bone injury with both carrying other health risks.  PRP injections so far have not shown much benefit in larger, high quality studies, however, some argue that this has come from variance in the quality of PRP used.  Time will tell the extent of benefit of PRP injection though it does seem that more evidence is emerging dissuading their use.

The British Journal of Sports Medicine released a good guide to treating tendinopathy on their blog that you can access HERE.

 

1.  Kubo, K., Kanehisa, H. and Fukunaga, T. 2002. Effects of transient muscle contractions and stretching on the tendon structures in vivo. Acta Physiological Scandinavica, 175: 157-164.

2.  Masci, Lorenzo. “Is Tendinopathy Research At A Crossroads?”. British Journal of Sports Medicine 49.16 (2015): 1030-1031. Web. 2 July 2016.

3.  Rees, Jonathan D, Matthew Stride, and Alex Scott. “Tendons – Time To Revisit Inflammation”. British Journal of Sports Medicine 48.21 (2013): 1553-1557. Web. 2 July 2016.

4.  Scott, Alex, Ludvig J. Backman, and Cathy Speed. “Tendinopathy: Update On Pathophysiology”. J Orthop Sports Phys Ther 45.11 (2015): 833-841. Web. 2 July 2016.

5.  Tilley, Benjamin J et al. “Is Higher Serum Cholesterol Associated With Altered Tendon Structure Or Tendon Pain? A Systematic Review”. British Journal of Sports Medicine 49.23 (2015): 1504-1509. Web. 2 July 2016.

6.  Wang QW,Chen ZL,Piao YJ Mesenchymal stem cells differentiate into tenocytes by bone morphogenetic protein (BMP) 12 gene transfer. J Biosci Bioeng2005;100:41822.

 

Conservative Treatment Ideas for Acetabular Labral Tears

There are important considerations for treating acetabular labral tears which can help guide patient care.

There is no doubt that acetabular labral tears are becoming increasingly common in sports medicine and rehab.  It is unknown whether the incidence is on the rise from increased or changing patterns of activity or if we are simply better at finding these lesions with improvements in diagnostic imaging.  It is likely a combination of each.  Regardless, rehab professionals should be prepared with a solid rationale for intervention strategies when treating individuals with labral tears.

Acetabular labral tears are typically caused by trauma or developmental etiologies.  The developmental causes often occur as linked to morphologic variance such as femoroacetabular impingment (FAI) and hip dysplasia.  Frequent aggravating movements of the hip can also cause and accelerate labral degeneration. 

cam pincer fai
 

The forms of FAI are seen above.

 

The vast majority of labral tears in western society will occur in the anterior-superior margin with anterior translation of the head of the femur contributing to labral overload.  The increased anterior translation of the femoral head occurs with excessive hip extension with standing or moving with hip hyperextension or in posterior pelvic tilt. Also remember that with external rotation we also get accessory anterior gliding. In individuals with excessive anteversion if they are to center the femoral head in the acetabulum, without compensatory tibial external rotation, they will walk with a degree of in-toeing. If they correct the in-toeing at the hip, the femur will be in a relatively externally rotated position with a propensity for increased anterior glide of the femoral head.  On the other hand retroversion has been linked to labral tears as the retroverted femur will more likely impinge the anterosuperior labrum with flexion especially when combined with adduction.  It is pertinent to assess femoral version.  Craig’s test has been shown both valid and reliable for detecting femoral version (studystudy.)

So with these considerations, here are some items to keep in mind when treating a patient with an anterosuperior acetabular labral tear.

  1.  Do not stretch into hip extension!  This should be pretty clear considering the location of injury and the mechanics associated with hip extension as mentioned above.  Stretching into extension will only further irritate the anterior hip as the femoral head will slide anteriorly in this position.
  2. Strengthen (and pattern) the glute max without driving the hip into hyperextension.  The glute max can help direct a posterior translation force on the proximal femur.  The glute max should be trained with attention to end range position avoiding driving into hip (hyper)extension.
  3. Address any posterior pelvic tilt.  As mentioned above posterior pelvic tilt can increase load to the anterior labrum.  Examine for possible causes of posterior tilt especially tight/stiff hamstrings and/or abdominals and weak lumbar erectors and/or iliopsoas.  The iliopsoas has been implicated by Lewis and Sahrman as a contributor to stabilization of the anterior hip during straight leg raise activity.  Weakness/inactivity in this muscle as compared to the rectus femoris may be noted in those with anterior labral injury as the rectus femoris will tend to translate the femur forward while the iliopsoas was modeled to stabilize the anterior hip.
  4. Perform gait analysis.  If an individual who has been determined to have increased anteversion walks with compensatory external rotation of the hip to walk with toes forward the femur will glide anteriorly.  I would not recommend teaching gait in a toe-in position even with anteverted hips, however, any out-toeing beyond neutral should be corrected in these instances.  Also assess for knee and hip hyperextension as marked by prolonged foot flat position late in stance phase.
  5. Limit isolated training of quadriceps and hamstrings, both of which can cause anterior translation of the femur.
  6. And finally good guiding principles of rehab are to simply avoid aggravating positions, strengthen joints and surrounding areas outside of the painful positions, and gradually reintroduce required and acceptable movements as tolerated by the patient.

For a good read on the topic see Shirley Sahrmann and Cara Lewis’s paper on the topic of labral tears. 

 

 

Mulligan Tape for Patellofemoral Pain

I have always attempted  patellofemoral pain (PFP) symptom modification with taping using only the McConnell method.  However, a recent study in the May 2016 issue of American Journal of Sports Medicine (Study) found that mulligan taping significantly decreased PFP and improved kinematics with decreased femoral internal rotation.  I think this new method of taping can potentially be quite useful for those individuals who do not respond to McConnell taping and whose comparable sign can be elicited with manual tibial external rotation or relieved with manual internal rotation during movement.

The Mulligan taping method involves applying rigid tape with an internal rotation force applied to the tibia.  The tape is wrapped from lateral to the tibial tubercle medially and superiorly above the knee ending on the posterolateral portion of the distal thigh.  Try it out with your patients and let me now if you find any benefit!

 

Time to Let Motion Palpation Die?

Unreliable, invalid, and creating a sense of fragility in patients. Does motion palpation deserve a place in clinical practice?

Having recently graduated from physical therapy school I can say that motion palpation is still being taught, but in a fettered or restrained manner consistent with the known unreliability of these methods.  It was approached as if we had to learn it because we would experience it in the real world from other clinicians, which we most certainly do, and as such we must understand the rationalization of their methods.  But somewhere along our clinical career paths many lose the skeptical mindset cautioning us of the unreliable, invalid premise of motion palpation and instead use the dated rationale unscrupulously ignoring that the practice of evidence based practice would preclude motion palpation.

I admit my bias against motion palpation originated immediately upon its presentation of physical therapy school with the known validity and reliability issues.  I recognize evidence based practice is not only comprised of scientific literature, but also clinical experience, and patient values.  I would argue, however, that each of these tenets of evidence based practice are compromised in this area.  Motion palpation is not just unwarranted because it is based on unvalidated concepts and unreliable techniques, but because it is inherently not in our patients’ best interest.  This comes not solely from the act of motion palpation itself or subsequent treatment, but in our attempt to explain why we are palpating and what we are correcting.

To explain this, I will use the common motion palpation surrounding the sacroiliac joint, an area of minuscule movement which clinicians have been attempting to feel for altered position and dysfunction for decades.  Let’s say a patient comes in complaining of pain around the sacroiliac joint.  A thorough lumbar, pelvic, and hip examination with use of the test item cluster for SI joint pain leaves you confident that the SI joint is the offending location.  At this point many will take to palpating the various landmarks of the sacrum and pelvis in vain attempt to detect any malpositioning of the sacrum or either innominate.  With this, validity has already flown out the door.  Landmarks on the pelvis and sacrum are known to normally vary based on normal morphology (See Study), which is observed both between sides in the same individual and between individuals.  Secondly, we know our hands are not sensitive enough to feel with any reliability the tiny (See Study) amounts of rotation or translation that would occur at the SI joint(See Study)(See Study)(See Study)(See Study)(See Study)(See Study)(See Study)(See Study), especially when we are palpating through the soft tissues around these landmarks.  Radiostereometric radiography with metal ball implantation into the pelvis is the only reliable method of assessing pelvic motion.  So despite the evidence we come to the conclusion that a specific malpositioning exists at the SI joint and a very specific intervention is required.  But this isn’t the truly bad part.  The bad part is that we then TELL the patient, in any number of concerning terms, that they were “out of place”-but not to worry because we can fix them.  So not only have we come to an invalid conclusion, but we use this conclusion to create a sense of fragility and dependency within the patient.  They now know to associate this pain they have with being “misaligned”, “subluxed”, “rotated”, etc. and that this issue can only be addressed with expert hands putting it back into place.  And just like that dependent, fragile patient created.  Does this sound like any model of healthcare you have heard of?  Hmm…

Let me clarify that I am NOT arguing against the notion of sacroiliac dysfunction nor am I arguing that the traditional treatment of SI joint pain do not get clinical results.  There is no doubt that clinicians using the motion palpation method and specific treatments of manipulation/mobilization and muscle energy techniques of SI “correction” can still have good clinical outcomes. In fact, there are some aspects in the methodology that resembles how I still treat some SI joint patients.  But this effectiveness can be explained a large number of ways that are not related to correcting positional faults.  We know manual therapy helps with pain despite highly tenuous biomechanical explanations (more likely neurophysiological in nature.)  We know that the muscle energy techniques are basically just isometrics; isometrics help with pain.  We often combine these strategies with other treatments including exercises (creating mindfulness and self-efficacy) and passive, pain-relieving modalities.  Therapeutic alliance, sense of expectancy, and placebo effects are also gained just by having the patient seen by a clinician who acts with empathy and care towards their concerns.  Not to mention that most musculoskeletal disorders simply get better naturally as a mechanism of regression towards the mean.  So while I still do manual therapy, muscle energy techniques, and other exercises for SI pain; My argument is that we must change what we are telling the patients.  We must stop telling them they are fragile, dependent creatures incapable of resolving pain without being put back into place.  It’s a load of BS and creates an unnecessary psychological burden on our patients and financial burden on the healthcare field.  We must recognize the pareidolia creating biased clinical reasoning and jeopardizing our patient’s physical and psychological well-being; it may be time to move past motion palpation.

Argument Against Biomechanical Explanation of Manual Therapy

Manual therapy is a mainstay in physical therapy and rehab but there’s a lot we we don’t truly understand about its mechanism of action.  We know it works; many studies show manual therapy has a positive influence on pain outcomes.  But how manual therapy works has not been clearly elucidated.  For those who have not critically investigated the details of manual therapy mechanisms will surely be quick to argue on behalf of biomechanical explanations.  But these mechanical effects really have not been clearly demonstrated in literature.  For example, did you know that it is really only possible to mobilize a joint in a direction completely perpendicular to the surface of the contact area on the skin.  This is because the skin-fascia interface is frictionless as found in a 2002 study in the Journal of Clinical Biomechanics.  This throws a wrench into the rationale of many thrust techniques that attempt to mobilize segments using variation in hand placement and force vectors.

I am not arguing that biomechanics absolutely do not matter in manual therapy.  However, I do believe that a more promising mechanism is that the forces applied in manual therapy initiate a sequence of peripheral and central nervous system neurophysiologic changes which positively modulate the pain experience.  Into this also plays the placebo effect, the effects of patient expectancy, and therapeutic alliance, all of which would contribute to the pain-relieving effects of manual therapy regardless of any mechanical explanation.  I think as clinicians we need skepticism to mechanistic explanation of our interventions, especially when the rationale for these interventions contradict basic scientific evidence.  We need to start considering how we educate patients and understand that if we use strict biomechanical explanations for our interventions we may perpetuate the patients’ perceptions of their bodies as fragile entities dependent on a clinician’s hands to “correct” their “misalignments.”  While this is good for business, and some businesses depend on creating a sense of fragility in the minds of patients,this is not good for our patients.  We should acknowledge that humans are innately resilient, adaptable, and capable of pain relief without being dependent on continual “correction” and “adjustments.”

Assessing Squat Form. Part 3

If you have not read the previous two posts on this squat assessment series read them (Here and Here.)

In this third and final blog on this topic I will discuss how we will take the considerations of body proportions and variation in mobility and motor control to individualize squat form.  As stated in part 1 our goal of this squat pattern is to achieve good depth while limiting lumbopelvic flexion to promote the ability to efficiently and safely move under loaded situations.

The first thing I do in a squat assessment is simply have the patient squat in their preferred position without cuing and note the quality of movement.  The qualitative judgement part does require some experience but you should have a general sense of when the squat looks off .  If it doesn’t look quite right, try following the steps below and you should arrive be able to determine what is limiting correct squat technique.  If the squat is nearly correct but some lumobpelvic reversal takes place in the bottom of the squat you may consider widening the stance a bit to see if this addresses the issue.  If it completely resolves the issue, then great, but I would still advise going through the steps below to rule out any concomitant limitations.

The next thing I do is to elevate the person’s heels and have them reattempt the squat.  This: 1)  Eliminates insufficient dorsiflexion from affecting the squat and 2) Shifts the person slightly forward to compensate for inability to “sit back” sufficiently during a squat.  “Sitting back” is a strength and conditioning term for moving the hip posteriorly and into flexion with an increase in corresponding forward trunk lean.  An inability to sit back can come from hip flexion limitations, hip extensor tissue extensibility issues, or a motor control issue.  Often if a patient exhibits this inability to sit back with hip flexion while maintaining good lumbopelvic position, it is a situation where the posterior chain muscles are actually stiff (artificially tight) in an attempt to impart stabilization to the lumbopelvic area in situations of reduce trunk stability.  So here it is important to recognize that “stiffness” is not the same as “tightness.”  Stiffness comes as a result of increased tone to stabilize a joint whereas true tightness comes from a shortening of muscles and their associated connective tissues often from maintaining positions of decreased tissue length.  This mechanism of stabilization is a primitive adaptation strategy because while it does improve the body’s ability to overcome the body’s overall external flexion moment it also predisposes the lumbar spine to excessive mobility requirements.  The topic of tightness vs stiffness is not a true dichotomy, however, as the two can exist in varying amounts at the same time.   Also to note,there is not a ton of abdominal strength required during a squat rather it is likely more a goal of stability and control.  A study by Stuart McGill showed surprisingly modest levels of abdominal musculature activity during functional exercises such as squats (Study.)

Now if the squat has improved with heels elevated you can assume that the problem exists with corrective explanations given in points 1 and 2 in the above paragraph.  To further the assessment I find it most useful (and simple) to begin with the ankle.  We must determine whether dorsiflexion insufficiency is hindering the squat technique.  To do this have the individual assume a half kneeling position in front of a wall with the forward toes about 4 inches from the wall.  Next have them lean the front knee forward towards the wall while keeping the heel down.  The amount of dorsiflexion achieved in this position is sufficient for any squat form.  If significantly lacking then dorsiflexion mobilizations and soleus stretching should be implemented before squat training.

If the ankle dorsiflexion test is negative, showing sufficient dorsiflexion, then we will assess the second point from above- the ability to sit back.  To check this have the patient perform a squat with the arms extended in front of them.  As mentioned in a part 2 this shifts the center of mass slightly forward which allows the squatter to remain slightly more forward and can decrease the amount of hip flexion and forward lean.  Next I compare this arms forward form with the squat form with a relatively light weight held against the chest.  This also shifts the weight forward but also acts to impart a flexion load to the lumbar spine which should engage the lumbar extensors and abdominals prior to movement.  If the form improves further with this strategy is likely that their exists a motor control issue involving the dissociation of hip and lumbar flexion.  If the form does not improve or only partially improves, I then look further into what is happening at the hip and lumbar spine.

I have the client supine on a table and perform an assessment of core stabilization using a comparison of the active straight leg raise and passive straight leg raise test.  During the active straight leg raise the client should begin with both legs extended straight.  The client then lifts one leg keeping both knees straight and the down leg in contact with the table.  Observe the active range of each leg and note whether the contralateral leg moved out of full extension.  Next perform a standard straight leg raise on each leg while palpating the anterior superior iliac spine to check for posterior rotation of the pelvis.  Stop the motion when pelvic rotation begins.  If the active straight leg raise flexion range of motion to the furthest point without contralateral hip flexion is significantly less (> 10 degrees) as compared to the passive straight leg raise to the point of pelvic rotation then there likely is a lumbopelvic stability issue.  This is because with poor stabilization of the lumbar spine during active straight leg raise the building tension in the hip extensors will cause an unchecked posterior rotation of the pelvis which will lift the contralateral thigh slightly off the table.

I then perform a gentle scour test on both hips to get a general sense of the hip shape and depth.  Typically you will notice that the hip achieves hip flexion much easier in a slightly abducting and externally rotated femoral position.  Check to be sure that sufficient hip flexion can be achieved, usually requiring 120 degrees for a parallel squat.  If passive hip flexion is limited in this position it is likely that limitations in the tissue extensibility of hip extensors is contributing to lumbopelvic reversal or lumbar flexion deeper in a squat.  Incorporating tissue extensibility and hip flexion mobilization should precede squat training if this is the case.

Next I have the patient quadruped on the floor or table and have them perform quadruped rocking observing the angle of hip flexion at which lumbar flexion occurs.  I then have the patient assume the same hip position as was determined to be the most mobile into flexion via the scour test above.  Greater hip flexion should occur and this gives you a good idea of where the person’s feet should be positioned during the squat.  If the patient has difficulty differentiating hip flexion and lumbar flexion in this position then you should coach them in this position until they achieve a feel for allowing the hip to flex while stabilizing the spine.

From here, I will use what I have observed to appropriately position the individual’s stance and then have them sit down onto a low box to get the individual in a near parallel squat position.  From the low box I use tactile cues to get the patient to achieve appropriate neutrality in their lumbar spine with some paraspinal muscle contraction if they have some amount of flexion.  I will have the patient cross their arms across the chest and lean forward, cuing them to keep thoracic extension, just until they are about to un-weight themselves from the box.  Here is where those strange proportions I talked about in part 2 may come into play.  If the patient happens to have very long femurs you will notice that they may maintain good lumbar position, exhibit satisfactory dorsiflexion, but they require a lot of forward lean to balance and require a ton of hip flexion due to having to sit way back.  These individuals may even look like their torso is nearly parallel to the floor.  In these cases you will need to adjust the width of the stance wider and continue to assess.  It comes down to clinical judgement on what you deem acceptable for squat form.  This individuals with disadvantaged proportions will do better with anterior loading, significant attention to maximizing dorsiflexion, and possibly even using elevated heel shoes to properly achieve parallel in the squat.

This is simply my method of assessing squat form and this manner is usually only done for those with grossly aberrant movements.  In those clients with form that shows only slight limitations they may benefit from immediate cuing or coaching to correct their form.  This should be done only if it is clear that mobility and stability impairments are not limiting the squat and that it is simply motor control.  Mobility and stability components are not directly influenced with cueing, only motor control is.  Furthermore, I also believe it is important to have the patient achieve a full squat pattern as outlined in Gray Cook’s FMS/SFMA systems.  This system would advocate training the full pattern before the squat pattern laid out in this blog series.  I do not necessarily disagree with the rationale of teaching the full squat before the “loaded” squat form, but I believe many clinicians will prefer to teach the mechanically efficient pattern I have described which allows for safe loading.

Feature Image from: Starting Strength 2nd ed. by Mark Rippetoe