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Treating the “I feel tight” patient.

We have all had patients present to us describing that some muscle “just feels tight.”  Often a perplexing finding on these patients is the lack of correlation to this sensation of being “tight” and loss of motion.  Some patients who show no perception of tightness show large losses of range of motion while some individuals who feel tight show normal range.  What is going on here?  It may very well be a protective neural mechanism creating a sense of tightness to constrain a perceived threat during dynamic activity. One of these threats to the CNS may occur when a muscle is impaired in production of muscular force at greater muscle lengths.  Notably, these individuals have terrible abilities to eccentrically lengthen their muscle to the same degree to which you can stretch them passively (perhaps relating to gamma motor neuron activity.. a thought for another day.) So let me give the example of the patient who presents with a sense of “tight” hamstrings.  These individuals never seem to be able to appropriately hip hinge to the same degree of hip flexion as you can passively take them in the analogous position of a supine hamstring stretch.  What I believe could be occurring in these individuals is that the perceived “tightness” is actually protective stiffness created from a subconscious response to perceived threat.  This threat may arise as a shift away from the optimal actin-myosin overlap represented in the plateau section of the length tension relationship (see image below.) As you move further right on the graph there is less available distance to elongate before potential fibril damage may occur…an understandable “threat.”

Active-length-tension1
Length Tension Relationship, from: www.strengthandconditioningresearch.com
What is required in these individuals is a shift of the plateau of the length tension relationship towards greater muscle elongation.  To do this there are two practical tools available: stretching and eccentric exercise.  Stretching has gotten a bad rap lately.  Acutely, stretching improves range of motion but typically for only a very short period of time (<60 minutes) with the most likely mechanism simply an increase in tolerance to stretch rather than any biomechanical effects(See study.)  Furthermore, stretching has come under scrutiny due to extensive literature demonstrating no improvement in injury rates and a decrease in muscle performance following stretching.  However, a recent literature review by Behm, Blazevich, Kay, and McHugh (See study) found that while static and PNF stretching did result in small (-3.7 to -4.4%) change in muscle performance this change is both dose dependent and able to be avoided.  Stretches held less than 60 seconds resulted in only a 1.1% decrease in performance with greater than 60 seconds resulting in a 4.6% decrease.  Additionally, performance decrease only occurs if the muscle is tested immediately after stretching with deficits in muscle performance effectively ameliorated with dynamic activity before exercise.  Chronically, stretching programs can cause lasting improvement in range of motion(See study) likely, in part, from the serial addition of sarcomeres, termed sarcomerogenesis, observed in several animal studies(See studySee study.)

So despite lackluster effects with acute bouts of stretching, stretching programs do appear to have a place in rehabilitation, though eccentric exercise may prove more beneficial in improving range of motion through sarcomerogenesis.  A 2012 review by Kieran O’Sullivan (See study) demonstrated that eccentric exercise programs are effective at increasing both range of motion and serial addition of sarcomeres.  Eccentric training allows muscular adaptation which can decrease injury risk and improve force production at greater degrees of muscle elongation (See studySee study.)  I always attempt to modulate threat perception using active muscle contraction at various joint ranges which is, in my opinion, why PNF techniques work so nicely at improving motion.  So while eccentric and stretching programs may both produce improvements in muscle length and flexibility (See study), it would make sense that eccentric exercise should be included with its ability to directly promote the ability to generate eccentric force at greater muscle length and for possible threat inoculation.  Keep in mind  this is about one factor that may contribute to threat, there are a multitude of others including constraining movement at a nearby body segment that are certainly as or more plausible.  In any case, if you don’t utilize eccentric training for range of motion improvement, for that, you should consider incorporating it into your repertoire.

 

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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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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.

What the Evidence Says about Acute Stretching

What do acute bouts of stretching actually do? Is stretching helpful or a hinderance when performed before exercise? Find out what the research says.

Stretching is component of health and performance governed largely by conventional wisdom with most people naive to what effects stretching has on performance, risk of injury, or even what stretching does from a mechanical or physiologic perspective. This blog summarizes the evidence from systematic reviews on a large number of research studies about the acute effects of stretching.

Acute Effects of Stretching

A recent systematic review by Behm, Blazevich, Kay, and Mchugh examined the acute (immediate) effects of static stretching (SS), dynamic stretching (DS), and proprioceptive neuromuscular facilitation (PNF) stretching on muscle performance, injury risk, range of motion (ROM) and the physiologic mechanisms underlying these changes.

First, let me quickly explain the difference in SS, DS, and PNF stretching. SS are stretches that are held at a certain muscle length usually to achieve some pre-determined degree of subjective “stretch” sensation. DS involves repeated movements to elongate a muscle through a pre-determined range of motion. PNF stretching usually involves one of two methods often done with the help of a partner. The first is contract-relax (CR.) Contract-relax is the use of a static stretch followed by an isometric contraction of the agonist muscle group (muscle being stretched) followed with relaxation into further stretch. The second method of PNF stretching is termed contract-relax, agonist-contract (CRAC.) This is the same as CR except when relaxing out of the isometric contraction the individual then attempts to contract the antagonist muscle while stretching the agonist further.

This review showed that acute SS does seem to slightly impair subsequent muscle performance variables with a dose dependent relationship. When stretches were held for less than 60 seconds a average weighted decrease between studies of 1.1% was noted in performance variables such as sprint velocity, jump height, and strength during knee extensor maximal volitional contraction. When static stretching was held greater than 60 seconds performance decreased 4.6%. It also appears that strength deceases are greater when a muscle is tested at shorter muscle lengths as compared to longer muscles lengths (-10.2% vs +2.2%.)

When looking at DS this review showed a weighted performance effect of improving performance 1.3% when averaged between studies. In general there were fewer studies that showed a negative effect of DS on performance as compared to those of SS. DS does not seem to have a clear dose dependent relationship in duration as SS does. Unfortunately there is large variation in the studies examined in terms of the amplitude of the dynamic stretches and few studies examined the frequency of the dynamic stretching movements so it is unclear of how the range of motion or the speed or frequency of movement might affect subsequent performance.

This review examined the effects of PNF contract-relax techniques and showed an average decrease between studies of 4.4% in performance despite most studies showing nonsignificant changes.  The review hypothesized that PNF stretching may follow similar patterns of a dose dependent response as SS with stretches less than 60 seconds resulting in less performance loss as compared to stretches held for greater than 60 seconds. There were 9 studies that actually compared the effects SS vs PNF and showed PNF had greater performance decreases (-6.4%) as compared to SS (-2.3%.)

The mechanisms underlying these strength losses are not completely evident but there is some evidence giving insight into this. One hypothesis is that changes in tendon stiffness may cause a muscle to function at shorter and weaker lengths. The review cites counter evidence to this with a study showing that the gastrocnemius produces less force following stretching despite being at the same length; this would suggest potential decreases in central (efferent) drive to muscles.

Another hypothesis provided is that mechanical stretching imposes stress into a muscle-tendon unit with the decreased blood flow, which occurs during stretching, possibly leading to increased metabolic end products. Animal studies have shown these end product accumulation in response to acute stretch, though this has not been examined in humans. It is also postulated that stretching may cause an impaired transmission of the action potential across the sarcolemma (muscle cell membrane.) And while there is evidence for a decrease in EMG in response to stretching, there is also evidence showing no changes in EMG; furthermore it is unclear how EMG would influence the transmission of electrical activity at the level of the sacrolemma. There is some evidence that there is a change in the efferent activity of motoneurons as a result in reduced facilitation from muscle spindles and would help explain why strength losses are greater at short muscle lengths.

The authors of this review did a good job of placing these performance decreases in perspective. Firstly, the performance measures were assessed on average 3-5 minutes after stretching; that is a pretty quick turnaround and likely not matched to what is done in sport. Secondly, the relative decreases in performance were quite small and may not even manifest themselves in changes in performance in sport or in more complex tasks. Thirdly, these changes may not persist if dynamic activity is performed subsequent to the stretching and prior to performance testing. However, if a concern still exists for decreased muscle performance from stretching interventions then one should consider incorporating dynamic stretching as there appears to be smaller deceases and perhaps slight improvements in performance subsequent to dynamic stretching.

The review also examined the effects of pre-activity stretching on injury risk. Twelve studies (SS or PNF, none used DS) were incorporated into the analysis with eight showing some effectiveness and four showing no effect; no studies showed any increase in injury risk. The reduction in injury risk is most evident when assessed in the context of sprint running-type sports as compared to endurance sports with a average risk reduction of 54% to acute muscle injury (as a side note, keep in mind this is a relative-risk reduction and not an absolute risk reduction. For example if hamstring strains occur at a rate of 0.27/1000 training hours then the subsequent risk would be 0.15/1000 training hours.)  All-injury risk reduction is less evident as pre-activity stretching does not seem as helpful in preventing overuse injury.

Perhaps the most commonly cited reason for stretching is to improve flexibility or to “decrease stiffness.” This relates to ROM improvements from stretching. The current body of literature does not support the notion of one method of stretching as being superior to another for improving ROM. Improvements in ROM are noted to be impermanent from acute stretching with increase ROM lasting anywhere from 5 to 120 minutes depending on the study.

This improvement in ROM from stretching is most attributed predominantly from an increase in tolerance to stretch, not necessarily a change in muscle stiffness; though evidence does exist towards both explanations. It is important to understand what is meant by “stiffness” as it is a scientific term relating to a stress-strain curve. Stiffness is the amount of force (stress) required to deform, or strain, a material. It is represented by the slope of a stress-stain curve; a simplified example I have constructed below.

Screen Shot 2017-10-20 at 4.41.53 PM

So the response to stretching is not to decrease stiffness which would manifest by shifting that curve to the right. Rather that curve remains the same, the individual is just able to tolerate going further along that curve into more strain (stretch.)

To summarize, while there does appear to be decreases in muscle performance in response to pre-activity stretching these values are very small and likely would not be too impactful in sport or performance in more complex tasks. Furthermore, these performance changes average about 1% when performed for less than 60 seconds, which, while significant in a research setting, would almost assuredly go unnoticed in normal performance situations. If you are concerned with the loss of strength or performance then dynamic stretching seems to be the way to go with potential, though very small, performance improvements noted. In terms of reducing injury risk, stretching does not seem to affect injury risk in endurance sports or for overuse injuries but does seem beneficial for reducing the risk of muscle injuries in higher velocity, repetitive movement-based activities. Range of motion is reliably increased with each type of stretching (SS, DS, PNF) with no clear superior method evident in the literature. The method of this improvement in range of motion is most likely predominantly from a perceptual change entitling more of an increase in tolerance to stretch.

So if you like to stretch before you train, continue to do so. If not, and you are performing sprint-like or high velocity movements then perhaps consider the use of either short duration static stretching followed by dynamic activity or by dynamic stretching. In my opinion, the most beneficial approach to pre-exercise activity is to perform a thorough warm-up with the goal of increase body temperature using movements that replicate those movements which will occur during training.

Stay tuned for another blog on the chronic effects of stretching such as with programs of stretching taking place over many weeks.

  1. Behm DG, Blazevich AJ, Kay AD, Mchugh M. Acute effects of muscle stretching on physical performance, range of motion, and injury incidence in healthy active individuals: a systematic review. Appl Physiol Nutr Metab. 2016;41(1):1-11.

 

How ACLs Tear

Anterior cruciate ligament (ACL) injury is the number one reason for time missed in sport with 100,000 -250,000 occurring every year in the U.S. alone (Hewett, 2016.) These injuries carry huge financial ramifications and increases rate of post-traumatic arthritis. Fortunately, risk of ACL injury can be quite accurately predicted and prevention strategies are shown to work well at reducing the incidence of injury and re-injury this.

–an important note: this risk is in reference to populations and not individuals; it is impossible to say exactly who will tear an ACL, but you can estimate risk within populations–

About 80% of ACL ruptures are non-contact injuries, with the athlete’s own movement strategies and muscle recruitment patterns causing the injury. Neuromuscular control programs indicate that at least 1/2 of non-contact ACL injuries can be prevented with neuromuscular training oriented at altering movement strategies (Gagnier, 2013)(Hewett, 2016.) These neuromuscular training programs are especially beneficial for at-risk females, as females are known to have altered neuromuscular control which places them at higher risk of ACL injury than men.

Non-contatct ACL injuries happen with rapid deceleration movements such as which happens with change of direction cutting, pivoting, and landing movements, especially when occurring in a single leg stance position. The ACL primarily restricts anterior translation of the tibia on the femur but also helps prevent hyperextension of the knee and gives rotational stability of the knee restricting tibial internal rotation (IR) more so than external rotation (ER.)

The amount of force required to rupture an ACL will vary individual to individual based on size of the ACL (larger individuals have larger ACLs) and likely genetic components. A study by Woo et al. showed younger cadaveric subjects, aged 22-35, had higher average strengths of the ACL with failure occurring around 2200 N of force as compared to 1500N and 660N for subjects aged 40-50 and 60-97, respectively. To put this into perspective 2200N (newton) is the force of about 220 kilograms with the accerleration due to gravity (roughly 10m/s^2.) Which is approximately the force of 485 lbs. This may seems like a lot of force, but consider that straight-line running can create ground reaction forces up to 3x bodyweight. Which means that a 200-lb male would create sufficient force to rupture an ACL with every step if it were to be transmitted into the ACL. Furthermore, the ground reaction forces within sporting events can be much greater than this. When these forces are directed into the ACL, it tears. Video analysis, computer modeling, and cadaveric studies have given us pretty solid evidence on how the ACL ruptures.

There is extensive evidence that now widely supports a triplanar ACL mechanism with knee valgus the common denominator. A 2014 study by Carmen Quatman revealed that loading of the ACL was greatest with triplanar motion involving tibial internal rotation, tibial abduction, and anterior tibial shear, though loads in her simulated falls using cadaver limbs were not sufficient to strain the MCL (Quatman, 2014.) This helps explain why only 4-17% of ACL ruptures occur with a concomitant MCL injury despite the MCL being the primary restraint to tibial abduction.

Video analysis of ACL injuries reveal they nearly always occur at knee flexion positions of around 20-30 degrees, which is actually quite a straight knee when viewed in the context of athletic performance (Koga, 2010.) It is not coincidental that this is the same angle we perform Lachman testing as ACL tension is greater in these positions of lesser knee flexion angles than when the knee is flexed more. An ACL rupture has been found to occur within 40 milliseconds of ground contact (Koga, 201o.) This is incredibly fast. About 3-4 times faster than the average reaction time for auditory and visual stimulus, and therefore, faster than what would be possible to sense and correct the risky position. This reveals the importance of appropriate preparatory movement and motor recruitment patterning. Observations of ACL injuries show the tibia internally rotating quickly in the first 40 milliseconds but then subsequently externally rotating. This change from tibial internal rotation to tibial external rotation is hypothesized to occur because of the loss of the ACL. A loss in the ACL’s ability to resist tibial anterior translation would cause the medial femoral condyle to shift backwards relative to the tibia with concomitant tibial external rotation (Koga, 2010.)

Muscle recruitment patterns can also help identify increased risk of ACL injury. Hamstring to quadriceps ratios (H:Q) have been used in the past as it is acknowledged that the co-contraction of the hamstring muscles create a posterior shear which offsets the anterior shear of the quadriceps and can decrease risk of knee injury, especially to the ACL. A quadriceps dominant landing strategy has been linked to increases in ACL injury (Zebis, 2009) Landing with a quadriceps dominant landing strategy not only increases the anterior shear of the tibia on the femur because of the line of pull of the quads, but it also is a strategy associated with landing on a stiffer leg and thus less knee flexion, which we also understand to be correlated with increased ACL loading and injury. Stiffer leg landing strategies are associated with greater relative quadriceps to hamstrings ratio and less overall hamstrings recruitment (Boling, 2013.)

Historically, hamstring to quad ratios (H:Q) have been used in terms of isometric strength but it may be more appropriate to consider the rate of torque development of the hamstrings as it is noted above and the quickness of ACL tear in response to GRF. It is observed that high peak concentric H:Q tend to be correlated to rate of torque development H:Q but the relationship is not always consistent(Greco, 2012.)

Side-cutting strategies have also been linked with increase rates of ACL rupture. Strategies of cutting in a wide stance and with trunk lean over stance leg show an increase in knee abduction moments and thus increase risk to the ACL (Kristianslund, 2014.) When the trunk flexes laterally over a plant leg the laterally displacement of the COM causes the ground reaction force, which is directed towards the COM, to pass now lateral to the knee which causes an increased knee abduction moment and predisposes to valgus collapse. Furthermore, landing with the center of mass located further from the base of support in the sagittal plane and with a greater limb angle (limb further from the vertical) is associated with increases in ACL rupture (Sheehan, 2012.)

It has been hypothesized that ACL tears could come from tissue fatigue failure, different from a traditional view of fatigue, whereby continual stress applied to tissue may cause eventual failure at the same amount of load which previously caused no harm. Fatigue failure has been demonstrated in MCLs of rabbits(Zek, 2010) and human extensor digitorum longus tendons (Schechtman, 1997.) A study in 2015 out of AJSM by Melanie Beaulieu suggests that ACLs can also fail from tissue fatigue which increases with limited femoral internal rotation with repeated landings (Beaulieu, 2015.) If the femur is not allowed to internally rotate then the relative internal rotation of the tibia on the femur will be much greater. Typically we want the amount of tibial rotation to be matched with the amount of femoral internal rotation. When the tibia accelerates into internal rotation relative to the femur then we increase loading of the ACL. The large valgus collapses we see in ACL injuries likely happen after the ACL has torn and partly because it has torn.

The best screening strategy would be do identify individuals using these movement patterns during dynamic activities. Four variables we are looking for during screening were summarized by Dr. Tim Hewett as ligament dominance, quadriceps dominance, trunk dominance, and leg dominance. Ligament dominance can be observed with inappropriate absorption of GRFs using a stiff legged landing and landings that are observed to coincide with increases in valgus collapse of the knee as mentioned above. Quad dominance is often observed with stiff legged landing strategies but can also be assessed with muscle testing and potentially with observation of movement patterns. Quad dominant individuals may display reduction in ability to hip hinge especially of note when the individual does not posterior shift their center of mass with athletic positions, but instead simply flexes the knee to achieve a lower COM. Trunk dominance, also termed core dysfunction, can be observed with single leg balance and cutting tasks. Tendencies for individuals to maintain balance on a single limb by laterally flexing their spine can cause ground reaction forces to pass lateral of the knee creating a knee abduction moment which can cause valgus collapse. When implementing return to sport/activity tests for patients returning from ACL reconstruction it is important to know how the ACL is torn and positions and movements which could load the ACL so we can appropriately screen for elevated risk. Keep these ideas in mind when rehabbing ACL patients.

 

 

Beaulieu ML, Wojtys EM, Ashton-miller JA. Risk of anterior cruciate ligament fatigue failure is increased by limited internal femoral rotation during in vitro repeated pivot landings. Am J Sports Med. 2015;43(9):2233-41.

Boling M, Padua D. Relationship between hip strength and trunk, hip, and knee kinematics during a jump-landing task in individuals with patellofemoral pain. Int J Sports Phys Ther. 2013;8(5):661-9.

Gagnier JJ, Morgenstern H, Chess L. Interventions designed to prevent anterior cruciate ligament injuries in adolescents and adults: a systematic review and meta-analysis. Am J Sports Med. 2013;41(8):1952-1962.

Greco CC, Da silva WL, Camarda SR, Denadai BS. Rapid hamstrings/quadriceps strength capacity in professional soccer players with different conventional isokinetic muscle strength ratios. J Sports Sci Med. 2012;11(3):418-22.

Hewett TE, Ford KR, Hoogenboom BJ, Myer GD. Understanding and preventing acl injuries: current biomechanical and epidemiologic considerations – update 2010. N Am J Sports Phys Ther. 2010;5(4):234-51.

Hewett TE, Myer GD, Ford KR, Paterno MV, Quatman CE. Mechanisms, prediction, and prevention of ACL injuries: Cut risk with three sharpened and validated tools. J Orthop Res. 2016;34(11):1843-1855.

Koga H, Nakamae A, Shima Y, et al. Mechanisms for noncontact anterior cruciate ligament injuries: knee joint kinematics in 10 injury situations from female team handball and basketball. Am J Sports Med. 2010; 38(11):2218–2225. [PubMed: 20595545]

Kristianslund E, Faul O, Bahr R, Myklebust G, Krosshaug T. Sidestep cutting technique and knee abduction loading: implications for ACL prevention exercises. Br J Sports Med. 2014;48(9):779-83.

Schechtman H, Bader DL. In vitro fatigue of human tendons. J Biomech. 1997; 30(8):829–835. [PubMed: 9239568]

Sheehan FT, Sipprell WH, Boden BP. Dynamic sagittal plane trunk control during anterior cruciate ligament injury. Am J Sports Med. 2012;40(5):1068-74.

Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-25.

Zebis MK, Bencke J, Andersen LL, et al. Acute fatigue impairs neuromuscular activity of anterior cruciate ligament-agonist muscles in female team handball players. Scand J Med Sci Sports. 2011;21(6):833-40.

Zec ML, Thistlethwaite P, Frank CB, Shrive NG. Characterization of the fatigue behavior of the medial collateral ligament utilizing traditional and novel mechanical variables for the assessment of damage accumulation. J Biomech Eng. 2010; 132(1):011001. [PubMed: 20524739]

Deficit of ankle dorsiflexion increases injury risk

Decreased dorsiflexion during landing tasks are associated with kinetics and kinematics that increase the risk of ACL injury according to a 2015 study (Malloy, 2015.) The study was conducted on 23 female collegiate soccer players. The study utilized a 3D motion capture system analyzing kinetic and kinematic data during a drop vertical jump. This data was then correlated to dorsiflexion flexibility measured using traditional goniometry in a knee extended position. It was found that significant negative correlations exists between dorsiflexion flexibility and peak knee abduction moments and knee flexion. This means that an ankle with more dorsiflexion range will experience greater knee flexion range of motion during landing and less knee abduction moment, which is the moment which would accelerate knee valgus. We know that landing mechanics that utilize a stiff leg strategy as well as those that increase knee abduction moments are correlated with elevated injury risk to the ACL. This study corroborates with previous studies showing similar findings. This information furthers the importance of acquiring dorsiflexion mobility in at-risk populations for ACL injuries especially those rehabbing from ACL rupture.

 

Malloy P, Morgan A, Meinerz C, Geiser C, Kipp K. The association of dorsiflexion flexibility on knee kinematics and kinetics during a drop vertical jump in healthy female athletes. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3550-5.

Caution against sidebending during single leg stance.

Watch out for individuals who stabilize in single leg stance by a laterally flexing their trunk. This trunk compensation occurs when an individual side bends at their spine to achieve a position of center of mass (COM) over their base of support. Preferably there would be more contribution from concomitant hip adduction and posterior shift of COM with slight hip flexion. The hip flexion position is important because it loads the hamstrings. There is significant evidence showing that stiff leg balance strategies and poor hamstring activation relative to quads to be predictors of injury particularly of the ACL. A laterally flexed trunk position over a single support is a risky position in sport as the laterally flexed trunk shifts the COM over the stance limb which directs corresponding ground reaction forces directly at the COM. With a laterally flexed trunk, these forces are lateral to the knee and thus create a external knee abduction moment (a force creating valgus collapse.) If you see your patient/ client balancing with a nearly straight knee and be leaning their body over the stance limb then this must be corrected and coached and should be observed to see if any maladaptive carryover has occurred in sport or practice.

Movement Patterns and SI Joint Pain

I have written previously about my belief in the error in practicing motion palpation surrounding the sacroiliac (SI) joint (see: Time to Let Motion Palpation Die?.)  A new paradigm of assessing motion of the SI joint was first introduced to me in the work of Richard Jackson, PT, OCS and Kris Porter, PT, DPT, OCS in the Pelvis and Sacroiliac Joint section of the Current Concepts of Orthopedic Physical Therapy guide.  Jackson and Porter describe that in light of the unreliable nature of assessing SI motion with palpation another manner of mobility assessment is desired.  One test suggested, while admittedly empirical, is a modified version of the Stork Test.  Traditionally, the stork test is performed by palpating the tested innominate’s PSIS and just medial to the PSIS of the same side.  The patient then flexes the hip of the test leg to 90 degrees while the pracitioner palpates for SI motion, with a normal finding said to be a inferior displacement of the PSIS.  As referenced in my article linked above these motion palpation tests are both woefully unreliable and invalid.  However, the modified Stork test, while not yet researched presents to me with better face validity.  Aberrant gross movement patterns are easier to identify and the evident, anatomical rationale implicates possible SI joint mobility restriction/ SI dysfunction.  During the modified Stork test, instead of placing the thumb on the PSIS you simply place your hands on each hip over the innominate bones.  The patient then again flexes the hip, allowing the knee to remain relaxed and flex as well.  A normal, or negative, test would show concomitant hip flexion with innominant posterior rotation, sacral extension, lumbar flexion, and slight spinal rotation towards the flexed leg.  With the negative test the hands will follow the pelvis into this normal posterior rotation without any compensations not listed above.  A positive test, however, will show a ipsilateral hip “hike” as the hip flexes as a hypomobile SI joint will not allow the posterior innominate rotation.  This presents as potentially more reliable as the “hike” is more easily observable than trying to feel with the thumbs the tiny movement at the SI joint.

Assessment of lumbopelvic rhythm is also suggested as a method of movement pattern observation lending some insight into sacroiliac joint dysfunction.  A normal lumbopelvic rhythm is traditionally said to occur with 120 degrees of motion, 60 from hip flexion and 60 from lumbar flexion.  Jackson and Porter site van Wingerden et al(2) who found individuals with pelvic pain had impaired forward bending.  Therefore, the observation may imply that those with pelvic pain will utilize a more spine dominant movement pattern and/or limited hip flexion during forward bending than those without pain.  It has also been demonstrated that individuals with pelvic pain will exhibit anterior rotation relative to the sacrum on the stance leg during single leg stance(Jackson and Porter.)  This has been described as a faulty movement strategy implicating faulty stabilization for load transfer.

I am note fully espousing these presented tests, however, I am suggesting that they show more promise than the antiquated and invalid idea of assessing and correcting postural flaws (rotations, upslips, downslips.)  The notion of using movement patterns to assess dysfunction is more encouraging as we know these gross movement patterns are more easily observed, although I fully disclose that these methods of assessing SI joint pain have not been validated.  It should be clear that these tests can reveal asymmetry in motor control and local and global muscular dysfunctions which can then implicate the tests as being, to an extent, both diagnostic and prescriptive.  If a patient shows movement pattern aberrancy during the modified stork test then we could conclude that exercise programming should eventually lead the patient towards the ability to stabilize the lumbopelvic girdle to promote the dysfunction in hip flexion.  While the exercises to accomplish this may be a bit more obscure and nuanced than this suggests, it still provides principle to treatment philosophy.

 

1.  Jackson, Richard, PT, OCS, and Kris Porter, PT,DPT, OCS. “The Pelvis and Sacroiliac Joint: Physical Therapy Patient Management Utilizing Current Evidence.” Current Concepts of Orthopaedic Physical Therapy. 3rd ed. APTA.

2.  van Wingerden JP, Vleeming A, Ronchetti I. Differences in standing and forward bending in women with chronic low back or pelvic girdle pain: indications for physical compensation strategies. Spine. 2008.