Athletes and Pathokinematics - Part III - Knee Injuries

As we saw in the previous blog last week, anything that alters the mechanics of the foot or the movements that occur at the foot can result in abnormal force attenuation and in a closed kinetic chain, where the feet are in contact with the ground we can see breakdown in any of the tissues and structures above the foot and ankle as well, including those in the lower leg.  We also discussed that many of the pathokinematics that we typically see at the foot and ankle are related to pronation, which we noted can result in abnormal force attenuation on not only the tissues of the foot and ankle, but also on those of the lower leg.  These effects, just as the effects on the foot and ankle, are also significantly increased during high impact sports due to the increased force required to participate in these types of activities.  Potential problems include, but are not limited to:

1.     Shin splints/stress fractures – shin splints or medial tibial stress syndrome refers to pain along or just behind the tibia.  This is a very common injury in runners and female athletes and occurs when there are repetitive high load activities that outpace the body’s ability to repair the tissues or the loads are simply too high for the body to resist.  Abnormalities in lower extremity biomechanics have been associated with increased incidence of shin splints.  If shin splints persist and the underlying mechanics are not addressed, this can lead to: 

a.     Tibial stress fractures – If the inflammation/pain is not resolved, the underlying mechanics or causative factors are not addressed and the activity continues, it can result in micro fractures of the tibia.  This can require prolonged care, casting and in extreme cases surgery.

b.     Anterior compartment syndrome -   in cases of shin splints and tibial stress fractures, it is important to monitor the athlete/patient for anterior compartment syndrome.  The anterior lateral portion of the lower leg is enclosed in a thick fibrous tissue called fascia.  This fascia encloses the anterior tibialis, extensor hallicus longus, extensor digitorum longus and the peroneus tertius muscles.  Along with this musculature, it also includes the deep peroneal nerve and the deep tibial artery.  Since the anterior compartment is an enclosed system, swelling in this area is of major concern due to the fact that it can compress the nerve and arterial flow to the lower leg and foot.  If sufficient enough and of long enough duration, it can cause permanent paralysis. 

2.     Pulled calf muscle— the calf is composed of the gastrocnemius and the soleus muscles.  A   With pathokinematics this is a common injury that can occur in runners and jumpers due to excessive foot pronation or limited flexibility of the calves.  Excessive pronation or decrease in dorsiflexion with running (from tight calves), can result in abnormal force attenuation at the calf or overwork.  Over time, this can lead to a tear or pull in the calf. 
pulled calf muscle can occur in either the gastronemius (more superficial) or in the soleus (more deep).

Pathokinematics Impact on the Knee: 

As we move up the kinetic chain, we see that the pathokinematics can also have as dramatic an impact on the knee as they do the foot and ankle.  As described previously, we typically see pathokinematics in one or a combination of the following movements at the knee: 

1.     Valgus stress at the knee (as a result of hip adduction). 

2.     Internal rotation of the femur on the tibia

3.     Genu recurvatum (hyperextension of the knee)

Occurrence of these in high loading situations or with high impact sports, can alter the articulations that occur between the bones or result in abnormal force attenuation on the tissues of the knee.  This can lead to several problems such as:

1.     Patellofemoral issues – the articulation between the patella and femur is the patellofemoral joint.  The patella rides in a groove in the femur from flexion to extension in a very predictable manner.  For this to occur in this predictable manner, the femur must remain in relatively “normal” alignment during closed kinetic chain activities.  When the femur falls into valgus, internally rotated or a hyperextended position, this changes the articulation between the two joints, potentially resulting in:

a.     Patellar tendonitis – the patellar tendon is a continuation of the quadriceps tendon and attaches the quadriceps to the tibia via the tibial tubercle.  When the knee moves into a valgus, internally rotated or hyperextended position, this places excessive tensile stress on the patellar tendon.  When this occurs over time and with high impact loads, the tendon can become inflamed (patellar tendonitis). 

b.     Patellofemoral syndrome/Chondromalacia – the patella rides in the femoral groove between the medial femoral condyle (MFC) and the lateral femoral condyle (LFC) as the knee moves from flexed   This groove is higher on the medial aspect (inside) than the lateral aspect (outside).  In order to maintain alignment of the patella in this groove with movement and to prevent abnormal wear between the groove and the underside of the patella, the knee must move in a somewhat predictable pattern.  Any variation in alignment of the femur on the tibia or change in the movement pattern in closed kinetic chain activities (valgus, internal rotation, hyperextension), can dramatically alter or change the contact area between the underside of the patella and the femoral groove.  If this occurs over time, this can result in wearing away of the articular cartilage between the two surfaces (chondromalacia) and ultimately result in pain (patellofemoral syndrome).
position to an extended position.

2.     Meniscal issues – the knee has two menisci (medial meniscus and lateral meniscus) that serve as   These menisci are designed to absorb compressive forces between the femur and the tibia and aid in preserving the articular cartilage of the femur and tibia.  The meniscuses, on the other hand, are weak when they are subjected to shearing forces and under these conditions they are more likely to tear.  Shearing force between the femur and the meniscus occurs when there is a valgus stress or rotational (internal rotation) stress imparted to the knee.   It is shearing forces that result in medial or lateral meniscal tears.  Over time and with increased severity of the tears, this can cause degenerative changes of the articular surfaces between the femur and the tibia (often referred to as degenerative joint disease).
cushions or shock absorbers of the knee.

3.     Ligamentous issues – the knee is composed of 4 ligaments.  The anterior cruciate ligament, the   Each one of these ligaments has a different function and force that they resist.  The two that are most commonly impacted with the pathokinematics described here are the medial collateral ligament and the anterior cruciate ligament.

posterior cruciate ligament, and the medial and lateral collateral ligaments.

a.     Anterior cruciate ligament (ACL) – the ACL originates at the medial border of the lateral femoral condyle and inserts on the tibia at the intercondylar area.  The ACL functions as a secondary static restraint to anterior translation of the tibia on the femur and hence aids in not only stabilizing the joint but also in protecting the meniscus from shearing forces caused by this kind of movement.  An ACL injury is a common injury in sports and in most cases will require surgical repair in order to facilitate full return to sport.  By design, the ACL is a good restraint to anterior translation however it is severely compromised when rotational (internal rotation) stresses are imparted to the knee.  Rotational stress creates a shearing force on the ACL.  In cases where there is a combination of internal rotation and valgus stress to the knee, creating both shearing force and tensile load, the ACL is compromised to an even greater degree.  This can result in either an avulsion of the ACL where part of the bone is torn away, (seen typically only in younger athletes), an ACL tear or an ACL rupture.

 

b.     Medial collateral ligament (MCL) – the MCL originates at the medial border of the medial femoral condyle and inserts at the periorsteum of proximal tibia, deep to the pes anserinus.  The MCL functions as a secondary static restraint to valgus stresses imparted to the knee.  By design, this ligament is stronger in tensile load situations but weak when subjected to shear loads.  With pathokinematics, this ligament is compromised in two ways.  When subjected to repetitive valgus stresses under high loading conditions, like those associated with sport, increased laxity in the ligament can occur over time.  This compromises its ability to resist subsequent high loads while simultaneously allowing increased gapping of the joint which increases the magnitude of the load imparted to the ligament.  When there is a combination of shearing stress (internal rotation) combined with tensile load, there is an increase in the potential for injury to this ligament.  This can lead to MCL pain, tears or ruptures. 

4.     Unhappy Triad – the “unhappy triad” terminology is used commonly in the sports medicine literature and community in reference to a common injury involving the ACL, MCL and the medial meniscus.  This injury typically occurs in sports from either a contact injury (where the knee is struck) or non-contact injury (usually during a planting and twisting motion).  It results from a combination of valgus stress in combination with internal rotation (shearing stress).  The typical course of treatment, depending on the severity of the injury, is ACL reconstruction along with repair of the meniscus tear.

5.     Iliotibial Band (ITB) Friction Syndrome – the IT band is a very thick and fibrous tissue that originates at the tensor facia lata (TFL) at the hip and runs along the lateral border of the femur to insert at the lateral aspect of the fibular head.  As the ITB transverses along the lateral tibial plateau, there is bursal sac that lies between the tibial plateau and the ITB.  ITB Friction Syndrome has often been correlated to tightness along the facial band and the TFL and is often associated with lateral knee pain.  This syndrome is commonly seen in runners. 

Next week we will look at the impact these movements have on the hip.  If you like what you read the biggest compliment you can give to us is to share the passion.  Follow us on Twitter @ACL_prevention or on Facebook at Athletic Therapy Services.  Remember #MoveRight, last longer and perform better!

Dr. Nessler is a practicing physical therapist with over 17 years sports medicine clinical experience and a nationally recognized expert in the area of athletic movement assessment.  He is the developer of an athletic biomechanical analysis and author of a college textbook on this subject.  He serves as the National Director of Sports Medicine for Physiotherapy Associates, is a Safety Council Member for USA Cheer National Safety Council and associate editor of the International Journal of Athletic Therapy and Training. 

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Athletes and Pathokinematics - Part II - Foot & Ankle

This week we will be looking at what is the impact of these pathokinematics on the various links in the kinetic chain?  To answer this question, let’s look in detail at the influence various types of pathokinematic movement patterns have on specific parts of the lower extremity, which for the purposes of this discussion will include the following:

·       Foot and Ankle

·       Lower Leg

·       Knee

·       Hip

·       Lower Back and

Sacrum

Pathokinematics Impact on the Foot and Ankle: 

Much like the analogy we used above with the car and tires, the foot is a very complex structure that is designed to be loaded in a very predictable fashion.  The foot is composed of 26 bones, 33 joints and over 100 muscles, ligaments and tendons.  It is the first shock absorber in the kinetic chain and its complexity of bones, ligaments, tendons, muscles, and joints, and the requirements made of it in order to allow the body to walk, run and stand, among other activities, mean that it must continually absorb tremendous amounts of force. 

Studies show that ground reaction forces, particularly as seen in high impact sports such as basketball, volleyball, cheerleading and gymnastics, can vary from 3 to as great as 6 times body weight[i].  Anything that alters the mechanics of the foot or the movements that occur at the foot can result in abnormal force attenuation with resulting breakdown in the tissues that can lead to acute or chronic injury.  In a closed kinetic chain, where the feet are in contact with the ground and we see pathokinematics at the foot or ankle, or anywhere in the body above the foot and/or ankle, it is easy to see the tremendous impact these poor movement patterns can have on the alignment and structures of the foot and/or ankle.

The pathokinematics that we typically see at the foot and ankle are often associated with pronation at the foot and ankle.  This can result in abnormal force attenuation on the tissues of the foot and ankle, the effects of which are significantly increased during high impact sports.  This can lead to several problems including, but not limited to:

1.     Plantar Fasciitis – the plantar fascia is a thick connective tissue which supports the arch of the foot.  Functionally, it serves to support the arch and to absorb force at the foot as the foot comes into contact with the ground.  Plantar fasciitis results from pathokinematics when the foot pronates excessively.  This results in the medial arch of the foot dropping more than it would normally or at a faster pace than normal.  This causes a significant tensile stress to the plantar fascia as well as a decrease in the amount of energy absorbed by the structure, for which it is partially designed, potentially resulting in two things:

a.     Excessive tensile stress over time can result in an inflammatory response in the plantar fascia called plantar fasciitis.

b.     Decreased energy absorbed here means that more force is then absorbed higher in the kinetic chain, beginning at the calcaneous, ankle, and moving to the knee, hip and lumbar spine. 

 

2.     Neuroma – a neuroma is a thickening or enlargement of a nerve.  In the foot, a common presentation of this is a neuroma of the intermetatarsal plantar nerve on the ball of the foot.  This is commonly referred to as a Morton’s Neuroma and presents as an enlargement, pain or tingling between the 3^rd and 4^th metatarsals on the plantar surface of the foot.  Athletes will often refer to this as pain at push off or a sense of a “BB” in the ball of their foot.  While these often result from foot deformities, flat feet or activities which cause repetitive stress to the ball of the foot such as high impact sports, pain, injury or excessive pronation (pathokinematics) can add to abnormal force attenuation of the forefoot and increased stress on the intermetatarsal plantar nerve.

3.     Retrocalcaneal bursitis – the retrocalcaneal bursa is a bursal sac that is between the calcaneous and the Achilles tendon.  Excessive pronation, causes increased tensile stresses to the plantar fascia and wear and tear on this bursal sac.  Excessive wearing over time can result in an inflammatory response which is referred to as retrocalcaneal bursitis.

4.     Achilles tendonitis and tendinosis – the Achilles tendon is tendon that attaches the gastrocnemius, soleus and plantaris muscles to the calcaneous.  Excessive pronation of the foot can result in excessive stress to the Achilles tendon resulting in tendonitis or tendinosis.  This can also be the result of several other conditions such as:

a.     Increased force attenuation – due to the increased pronation at the foot and a resulting decrease in force that is absorbed by the plantar fascia, mid-foot and rear foot, the Achilles tendon is then exposed to higher forces.  Over time this can result in tendonitis (inflammation of the tendon) or tendinosis (a long standing problem where there is breakdown of the collagen, scar formation or calcification) of the Achilles tendon.

b.     Prolonged or worsening plantar fasciitis - the plantar fascia is continuous with the Achilles tendon via the fascial sheath and as a result, excessive stresses to the plantar fascia, prolonged and or worsening plantar fasciitis can often result in Achilles tendonitis.  The knowledge of this connection is often used in treatment of plantar fasciitis.  Knowing this, if the toes are dorsiflexed, the plantar fascia tightens.  If a tensile force (stretch) is then generated in the Achilles tendon, it will increase tensile strain in the plantar fascia and vice versa. 

c.     Pain – pain resulting from plantar fasciitis or retrocalcaneal bursitis (as the result of excessive foot pronation) can result in compensatory movement or gait.  These additional compensatory movements, in themselves, can add to an already increased force attenuation at the Achilles tendon.

Consider a case study for an in-depth look at the impact pathokinematics can have on the foot and ankle.  At left is a cheerleader who demonstrates a significant lateral shift when squatting.  At the end range of motion of her squat, she loses control at both ankles, and excessively pronates into pes planus.  This is much more evident on the right than the left in this photo.  The athlete here is highly trained and very fit, but complains of ankle pain, especially on the right with competition.  She also complains of difficulty reaching peak vertical height when jumping as a flyer.  Obviously, in cheerleading, this is an important measure of success overall, and is critical for many specific cheerleading activities.

This individual also demonstrates a significant lateral shift when descending (eccentric movement) as well as with ascent (concentric movement) during the squatting motion, which is indicative of decreased lumbopelvic proprioception.  If combined with adduction of the hip during single leg squat movements, this can indicate gluteus medius weakness on one side.  Since she demonstrates excessive pronation bilaterally with squat and with a step up motion, we can also suspect weakness in the musculature of the foot, ankle and lower leg.  Weakness in this area can cause extreme pes planus during these motions and add to the hip adduction we see in single leg squatting motions.  In this example it is evident that the right is weaker than the left, secondary to the magnitude of pronation. 

Because the ankle is a hinged joint, it is designed to move the foot in four primary directions:  plantar flexion, dorsiflexion, inversion, and eversion.  When the foot is forced to pronate to this degree, as in this example, there is a tremendous amount of stress on the tendons and ligaments of the joint which serve to stabilize it in all three planes of motion.  These include the anterior talofibular ligament and calcaneaofibular ligament as well as the peroneal tendons, and the Achilles tendon.  The gastrocnemius and soleus calf muscles that attach at the ankle, as well as the calcaneus and retrocalcaneal bursa are at risk as well.

So what kinds of injuries is this athlete likely to incur?  She certainly is at risk for ankle sprains, stress fractures (shin splints) and fractures, especially upon hard landings from jumps.  She is also subject to tendonitis or inflammation of the tendon, which can occur in the Achilles tendon, the posterior tibial tendon, or the peroneal tendon in this case.  If tendonitis occurs, especially in the Achilles tendon area and the athlete does not rest, there is increased risk of the tendon rupturing or tearing, which usually requires surgery to repair.  Other possible injuries this athlete could sustain include breaks to the metatarsal bones (toes), the calcaneous (heel bone) or lateral or medial maleolus, or tearing and/or inflammation of the plantar fascia.  Because of the loss of kinetic energy across the system, and the associated adduction of the knee in a closed kinetic chain, this athlete could also be more susceptible to injuries of the ACL and medial and lateral meniscus at the knee which have to work harder due to an unstable surface at the foot and ankle. 

As noted before, this athlete will be limited on peak vertical height when jumping as long as the kinetic chain is interrupted in this fashion, and energy is absorbed at the ankle instead of passing through the foot to the ground upon take off.  Her endurance will be similarly limited because of a lack of symmetrical strength in the lower extremity and the greater force that is required to obtain heights that would normally not take as much force.  Her ability to participate effectively in stunts that require jumping and bounding motions is therefore compromised.

 
Next week we will look at the impact these movements have on the knee.  If you like what you read the biggest compliment you can give to us is to share the passion.  Follow us on Twitter @ACL_prevention or on Facebook at Athletic Therapy Services.  Remember #MoveRight, last longer and perform better!

Dr. Nessler is a practicing physical therapist with over 17 years sports medicine clinical experience and a nationally recognized expert in the area of athletic movement assessment.  He is the developer of an athletic biomechanical analysis and author of a college textbook on this subject.  He serves as the National Director of Sports Medicine for Physiotherapy Associates, is a Safety Council Member for USA Cheer National Safety Council and associate editor of the International Journal of Athletic Therapy and Training.  

Athletes and Pathokinematics - Common Injuries

In this blog series, we will look at several common pathokinematic movement patterns seen in athletes and discuss the influence these have on joints, ligaments and muscles.  We will also review a few of the more commonly seen injuries that can result from these abnormal movement patterns in the lower extremity and touch on a few related performance issues that can also arise when pathokinematics are present and the kinetic chain is compromised.

 

To give an overview in order to begin this discussion, let’s look at one of our previous examples.  This athlete, photographed as she jumps in a forward direction demonstrates several severe forms of irregular or pathokinematic movement patterns:  hip adduction, internal femoral rotation of the hip, genu valgum at the knee and bilateral “toeing in.”  Although this case is extreme, it is not completely abnormal to see these types of movement patterns, although perhaps to a lesser degree, in a competitive athlete such as this one.  The research has shown that these types of movement patterns are highly associated with increased stress to the hips and to the knee (in particular the ACL).  Even the casual observer can see how there would be increased stress to both ankles, both feet (plantar fascia in particular) and the lower back as well.   Specifically, this athlete is at risk for a number of common athletic injuries.  Based on her movements alone, she has increased stress to the:

 

 

1. Big toe – increased stress to the 1^st metatarsal with increased load to the bone when landing which could result in bone bruising
2. Plantar fascia – with this landing position of the foot, there is considerable stress to the plantar fascia which can result in plantar fasciitis
3. Knee - with rotation and valgus stress at the knee there is increased stress to the ACL, the meniscus within the joint, the lateral illiotibial band insertion and patellofemoral joint, which can result in ACL tears, meniscal tears and illiotibial (IT) Band Friction Syndrome
4. Hip – the internally rotated position of the hip increases stress to the labrum, femoral head and trochanteric bursa, which could result in labral tears, stress fractures and trochanteric bursitis
5. Lower back – with excessive movement in the spine and the adducted position of the hip, much greater stress is exerted on the sacroiliac joint and the L5/S1 vertebra, which could add to S1 joint pain, and to wearing of the L5/S1 intervertebral disc and facet joints. 

Why would this be so if these are the established patterns of movement for this individual?  Pathokinematic movement patterns such as those in this example result in forces being distributed throughout the system or along the kinetic chain, in an abnormal fashion—in other words, in a way that is different from the way the system was designed to absorb force.  We refer to this as abnormal force attenuation and over time abnormal force attenuation can lead to various injuries along the kinetic chain, all the way from the foot and ankle up the chain to the lumbar spine.  Attenuation is defined in this case as the gradual loss and ultimately the extinction  of energy (force) as it travels through a medium, in this case the lower extremity of the human body. 

Much like a car is designed to have optimal performance when the weight distribution is equal across all four tires, the human body is designed to perform optimally when it absorbs force equally at the two places it touches the ground—at the feet.  This enables the structures of the body to equally distribute and put those forces to use for efficient movement with the least amount of destructive stress placed on the muscles, joints, ligaments and tendons of the body.

In the human body, during movement and in sports, loading variations from the “optimal position” can and do occur under certain circumstances.  This is common and, through proper conditioning, injuries can be avoided during high load or force situations.  However, if loading variations that distribute force unequally across the lower extremity become the norm or the predominant way the tissues are loaded over time, structural imbalances can occur that create wear and tear on the structures of the body and can lead to injury.

Injuries occur when the breakdown of tissues (from abnormal loading in this case) outpaces the body’s ability to repair those tissues.  Looking at this more closely, when force is distributed in an abnormal fashion a majority of the time, especially under high impact loads or forces, the body’s or tissue’s ability to respond quickly to and resist breakdown is compromised.  Using the analogy of the car, if your tires are low on one side for a short period of time, then the vehicle and tires usually sustain no damage.  When you fill them up to optimal air pressure, weight distribution is restored to normal and there is no damage done.  But, if your tires remain low on one side for a long time, then irreversible damage can be done to the tires, the shocks, the axle, etc.  Because the human body is a living organism, which is constantly adapting to environmental stresses and repairing itself, it can often resist abnormal forces for many years prior to showing the signs or symptoms of injury.  This is why in so many cases abnormal movement patterns are not noticed until after serious injury has already occurred.

One question in considering movement patterns as they relate to injury and vice versa, is whether or   Is it the chicken before the egg or the egg before the chicken?  Was the movement pattern there prior to the injury or did the injury result in, or cause, the poor movement patterns.  That definitive answer to this question remains unknown, but it could be either or both. 

not pathokinematics cause injury or injury causes pathokinematics.

This can also be true with some of the other pathokinematics that we discuss.  For example, many times we see patients or athletes who have developed a lateral shift with a squatting motion.  This compensatory movement can be the result of the individual attempting to move away from the side the pain is on but still accomplish the movement.  For example, if an athlete has pain in the right knee with squatting greater than 60 degrees, then he or she may demonstrate a left lateral shift when squatting to 80 degrees of knee flexion.  This allows him or her to accomplish the motion but at the same time avoid pain in the right knee.  Once the pain is resolved, the lateral shift often corrects itself, without the need for further intervention. 

However, in some cases, these types of pathokinematic movement patterns will not self correct when the source of pain is addressed.  If in fact, they do not and the athlete carries the same pathokinematic movement patterns over to daily and/or athletic activities once the pain issue is resolved, then we can say that this movement pattern is likely no longer simply a compensatory strategy to avoid pain.  This movement pattern, or the “motor plan” that results in certain ways of moving, is the result of changes within the primary motor cortex.  In other words, the abnormal movement, over time, has resulted in a motor program which has become ingrained in the primary motor cortex and is the primary program to which the brain reverts in order to generate this particular movement whenever it is needed. 

Therefore the lateral shift during a squatting motion can become the “natural” program which the brain uses for all subsequent squatting motions.  Despite the decreased efficiency of such a movement and the abnormal force attenuation that it will impart to the tissues, it will remain the primary program the brain will use unless it is re-trained otherwise.  The program must essentially be “re-written” in some way, rehearsed and relearned over time.  So, much like the baseball pitcher who has developed poor throwing habits that we talked about in an earlier chapter, poor movement patterns like these must be retrained in order to be permanently corrected.  Just like correcting a pitcher’s pitch, new movement patterns, once relearned, must be reinforced over and over again in order to “reprogram” the brain to automatically move in this way when required.

Although some of the pathokinematics we describe result from compensatory movement to avoid pain or weakness, or are movements that have become programmed in the primary motor cortex over time for some reason, there some pathokinematic movement patterns which do not fall into either of these categories.  For example, the hip adduction and internal rotation that occurs with jump stops or single leg squats are not the result of compensatory strategies.  Since these movements result in abnormal stresses to tissues (such as the shear stress to the ACL or meniscus during jump stops) and are more likely to cause pain as opposed to relieving pain if present, then these are more likely the result of other factors. 

In many cases, these types of movements are the result of many factors in combination such as muscle weakness, or tightness, poor proprioception or the development of poor movement habits (perhaps due to pain, injury or improper instruction) earlier in their career.  If these movement patterns are never addressed and corrected, then they will continue and eventually become part of the primary motor plan as well.  Over time, this can result in even greater asymmetries in strength, continued or increasingly abnormal recruitment patterns (sequence by which muscles are activated) and an even higher increased risk for injury.  Regardless of the causative factors, if not corrected, pathokinematics ultimately result in abnormal force attenuation throughout the kinetic chain.  This will break down the structures of the body and can lead to pain or injury, which then can lead to additional or more exaggerated pathokinematic movement patterns.  Ultimately, this order of events can eventually become part of a “vicious cycle” leading to additional pain/injury, even more avoidance-related movement patterns, and new and more widespread weaknesses.

 

Next week we will continue this discussion by looking at the impact this has on common athletic injuries of the lower kinetic chain.  If you like what you read, the biggest compliment you can give us is sharing the passion.  Follow us on twitter @ACL_prevention or follow us on Facebook at Athletic Therapy Services.  Remember,  #MoveRight and last longer and perform better.

Dr. Nessler is a practicing physical therapist with over 17 years sports medicine clinical experience and a nationally recognized expert in the area of athletic movement assessment.  He is the developer of an athletic biomechanical analysis and author of a college textbook on this subject.  He serves as the National Director of Sports Medicine for Physiotherapy Associates, is a Safety Council Member for USA Cheer National Safety Council and associate editor of the International Journal of Athletic Therapy and Training.  

 

We Are On The Edge - Will We Take The Jump???

For this series, I am going to stray from my traditional route of literature review and share more of a personal perspective.  In the last month I have been blessed and humbled with opportunity to take a new and exciting direction in my professional career as a national director of one of the nation’s largest sports medicine programs.  This opportunity is providing me with the exposure to some really exciting things happening in our respective professions.  Things which, I hope, will forever change the world of sports medicine.  Forever change the way we, as coaches, athletic trainers and physical therapists and physicians approach and look at our athletes.

Back in 1998 -2000 I felt a true calling and passion to do something about youth athletic injuries.  It was the 22 ACLR patients that came into my office over a 2 week period that inspired me to do something about this horrific epidemic.  Since then, I have written numerous articles, published papers, authored a college textbook and developed a technology to assess movement in athletes to reduce risk for injury.  All of this with little personal gain other than knowing that I am serving the calling that I was called to do.  To know that in some small way, I may contribute to one child not suffering a non-contact ACL injury makes this whole journey worth it. 

Throughout the last 15 years, what I have learned is that the long term health impacts are devastaing and that we cannot leave it up to someone else to come up with a solution but we must drive the innovation and solution ourselves.  If you have followed this blog, what I hope you find is research based education which you can take back to the mat and apply with your athletes.  But reading alone is not enough.  WE have to be willing to make the jump!  This is my call to action for you.  To impact this epidemic, we must be willing to push ourselves to the next level and do something different if we ever expect to change the current trends.  The research is clear.  It has been out there for over 15 years.  WE know what we should do, now IT IS THE TIME TO DO IT!

One thing I would ask you to consider, is question the logic.  So many times we rely on others to come up with the solution.  We take courses from them, we read their books and buy their materials.  But many times there is the question lingering at the back of our heads of does this make sense.  Sometimes it does not and yet we want it to make sense.  Often in these situations we find ourselves defending the logic despite the research indicating the opposite.  Perfect example is I recently tweeted the following tweet:

I received a back lash of messages from people loyal to this test but the reality is this, this test is not sensitive to measuring asymmetry.  This test also does not measure the number one indicator that the literature tells us that puts athlete’s at risk for injury.  Myers et al, AJSM 2012, showed that single limb performance is the best indicator of non-contact injury risk.  Kristinaslund et al, AJSM 2013, showed that single limb performance best represents how the limb will respond

during athletic participation.  More recently, Rohman et al, AJSM 2015 showed that limb symmetry index is the best indicator of limb ability in sport and good for injury prediction.  So why is it that we are not assessing this in a profound way?  We also know from Tong et al, Phy Ther Sport 2015 that the endurance plank test is a valid, reliable and practical test for assessing global core muscular endurance in athletes.  Yet one of the most common test we use is the rotational stability test.  Yet, support for the rotational stability test’s correlation to core stability let alone correlation to sport is not supported in any peer reviewed journal.  If this is the case, why are we not looking at plank testing in athletes. 

So, it is not that I am for or against this particular test, but I am for what the research tells us.  What the research clearly tells us is that there is a better way of doing things.  Just because that is the way we currently do it or have done it does not mean it is the way we should continue to do it.  Research tells us what we should be looking at.  The interesting thing is that what the research is telling us make sense when you think about it.  So, do we continue to do what we have been doing with limited results or do we break out of the box and truly look to change the way we assess and treat our athletes. 

The beauty of 2015 is the technology revolution that we are in.  If you are not using technology in your sports medicine practice, you will soon be outdated.  Technology affords us new, more efficient and much more reliable ways of assessing what we should be looking at.  Study after study shows that the eye ball is good but intra/inter-rater reliability with many of today’s movement assessments is just not there.  If we can integrate movement assessment with technology, would we see a more dramatic reduction in injury rates?  Or are we content just doing it the same way we always have despite the research and the tools that are available to us?

I hope you sense the passion.  But what I really hope is that what you will see over the course of the next 12-18 months is some serious change in the way that we do things.  In this new role, we will use the research to drive the interventions that we provide.  We will directly measure the outcomes of the athletes we treat and use those outcomes to drive future education and innovations in the way we treat our athletes.  We will be cost conscious to the health care expense and at the same time drive improved outcomes, improved athlete experience, reduced recitivizm (rate of re-injury) and improve athletic performance!   

As basic as it sounds, to truly change movement, we must change the way that we think.  And although it is not 100% data driven, it is 150% science driven.  Over the course of the next month, I will be providing excerts from our textbook to help us all understand better the sciences behind movement and why we should do what we should do.  And that is, assess it better.  Move better, feel better, perform better and last longer.  That simple!   If you like what you see, SHARE THE PASSION!  It is the biggest compliment you can give.  Follow us on Twitter @ACL_prevention and tweet about it.  #MovingToChangeMovement and help us spread the passion.

Trent Nessler, PT, MPT, DPT:  Physical Therapist | Author | Educator |Innovator in Movement Science and Technology.  Dr. Nessler is a physical therapist and National Director for Sports Medicine for Physiotherapy Associates.  He serves as an injury consultant and is actively involved in movement research.  He has been researching and developing movement assessments and technologies for >10 years is the author of the textbook Dynamic Movement Assessment: Enhance Performance and Prevent Injury, and associate editor for International Journal of Athletic Therapy & Training.  You can contact him directly at trent.nessler@myphysio.com

If The Patient Can't Feel It, They Won't Change It! - A Guest Post

Over the course of the last several years, I have been blessed to come across some amazing people in our respective professions.  People who are doing some very innovative things in technology, research and movement.   One of those individuals is Eric M. Dinkins PT, MSPT, OCS, Cert. MT, CMP, MCTAAs.  Eric is a practicing clinician, educator and innovator in the movement sciences.  In 2014, Eric and a colleauge started a company called motion guidance.  A technology designed to assist patients and athletes in correcting pathological movement patterns.  I am honored and humbled to have Eric doing our guest blog this week.

If the patient can't feel it, they won't change it   

I may have slept through this lecture in PT school, but early on in my career I often mix balance and proprioception into the same definition or would at least train them the same. Although my first job involved the rehabilitation and training of high level athletes, the implementation of balance and proprioception often overlapped. In hindsight, the reality is that most high level athletes get better with rest and some moderately skilled manual and exercise treatment. Not to say that the treatments weren't skilled, but the vast majority of injuries progressed with very similar treatments.

But with time and experience, it was those intermediate, competitive athletes that would see failures; at least never return play how they considered their pre-morbid level. Often the return to play would involved continued muscle spasm or that low grade ache that, while not preventing them from competing, would yield hesitation or decreased performance. Re-evaluation would demonstrate normal ROM, strength and functional movement screen. It was at this time that I delved back into what I may have been missing and how I could clean this up. And I noticed that I was ignoring that differences between balance and proprioception. Especially in head, neck and shoulder injuries.

Proprioception involves that conscious AND unconscious understanding of a joints position in space, movement, and force sense. It is processed at all levels of the CNS and is integrated with other body systems like the vestibular, visual and somatosenory systems. Mechanoreceptors are specialized nerve endings that process this sensory information and convert this input into action potentials to be sent to CNS for processing. According to Proske and Gandevia, 2012, the most important source of proprioception is considered to come from the muscle spindles found in skeletal muscle. The suboccipital muscles have a high density of muscle spindles, thought to reflect the exceptional coordination role in head and eye movement control. Proprioception is also important after movement has occurred for a comparison of intended movement vs actual achieved movement. This comparison is vital for motor learning to occur by updating the internal forward planning model of motor commands. 

Proprioception can be altered or impaired by several factors. Pain, fatigue, joint effusion on the capsule, and trauma to structures all can change our proprioceptive awareness and thereby changing the motor control pattern in which our body systems work together to be most effective. Disturbed feedback, feedforwrad, regulation of muscle stiffness, postural stability in balance, visual acuity, and joint stabilization can all be affected with changes to the body's proprioception.  Despite the substantial importance of proprioception for body function, most clinics have a paucity of tools to accurately assess proprioception.

Several research articles have stated that exercise augments proprioception via activation of muscle spindles. I'm sure this is why so many of my athletes would succeed early on in my career. Exercise would naturally retrain the proprioceptive losses from injury and body awareness would return without specific re-training. But various exercises activate receptors at specific levels of the CNS that can differ between individuals. Thus leaving some patients without the proper training to re-educate their proprioception. If not properly re-educated, the body may continue to interpret certain inputs as a threat and produce abnormal responses.

This is where I enjoy using motion feedback (like the Motion Guidance device). Both for clinical assessment of how people like to move as well, interpretation of if that movement (or lack of) is abnormal or necessary, and visual feedback for the patient immediately as they are moving. Many of my patients present in clinic without being able to reproduce their primary symptom that may warrant them to be in my office anyway. What is left is an educated guess on what movement patterns, weakness, overload, environment, etc may be contributing to their pain. Motion feedback allows me to see a piece of what might be contributing to their pain more accurately that with the naked eye. And helps bridge the gap between the novice and expert clinician. It gives clinicians an extra clinical assessment tool for proprioception, preferred movement patterns, and development of motor learning. This is most evident in the use of laser feedback regarding Joint Position Sense. Chen and Treleaven in 2013 researched the use of a laser to determine accurate JPS in whiplash patients and it was found to be reliable and valid (1). Simple observations of errors on a target determined whether the subject had altered cervical proprioception. Balke found similar alterations in changes for proprioception of the unstable shoulder in 2011(2) . Hande et al also found knee JPS loss was correlated with both quadriceps eccentric and concentric strength among patients with PFPS (3) .

1) http://www.ncbi.nlm.nih.gov/pubmed/23810427

2) http://www.ncbi.nlm.nih.gov/pubmed/21350968

3) http://www.ncbi.nlm.nih.gov/pubmed/25869907

Perhaps the most valuable aspect of attempting to define and objectively measure proprioception is ultimately how we see, or don't see the body move. Having the ability to accurately determine a preferred motor pattern or attempt to correct a faulty one comes down to proprioception. If the patient can't feel it, they won't change it. There are biofeedback tools that are available to clinicians to improve the learning curve, such as the Motion Guidance device, the Dynamic Movement Assessment, or clinicians can use garments, tactile cues or mirrors to assist in understanding an individuals propriocepetion. But these tools are only extremely valuable if the information or data collection yields learning by the patient. The old saying of “you can lead a horse to water, but you can't make it drink” really applies to this scenario.

As “movement science specialists”, the sports and healthcare professionals involved in rehabilitation MUST be able to understand and diagnosed movement. But it goes further. It is imperative to convert this information into lay terms that the patient can use to interpret what is necessary to create change in their movement. This change, whether addressing JPS, weakness, FMP, tissue overload, etc, is what needs to be owned, understood and acknowledged by the patient. This is all effecting proprioception! Otherwise, change will not happen. If the patient can't feel it, they won't change it! One of our job as rehabilitation professionals is to help our patients learn.

I think Eric would agree, but as basic as it sounds, to truly change movement, we must change the way that we think.  Move better, feel better, perform better and last longer.  That simple.   If you like what you see, SHARE THE PASSION!  It is the biggest compliment you can give.  Follow us on Twitter @ACL_prevention and tweet about it.  #MovingToChangeMovement and help us spread the passion.

Trent Nessler, PT, MPT, DPT:  Physical Therapist | Author | Educator |Innovator in Movement Science and Technology.  Dr. Nessler is a physical therapist and owner of Athletic Therapy Services.  He serves as a practicing clinician and movement change consultant for practices and organizations looking to develop injury prevention initiatives and strategies.  He has been researching and developing movement assessments and technologies for >10 years is the author of the textbook Dynamic Movement Assessment: Enhance Performance and Prevent Injury, and associate editor for International Journal of Athletic Therapy & Training.