Have you seen this?

Patterns. That’s what it’s about a lot of times. Dr Allen and I are always looking for patterns or combinations of muscles which work together and seem to cause what appear to be predictable patterns; like a weak anterior compartment and a weak gluteus maximus, or a weak gluteus medius and contralateral quadratus lumborum.

Here is an interesting story and a new combination that at least I have never seen before

I had a 11-year-old right footed soccer player from my son’s soccer team coming to see me with bilateral posterior knee pain which began during a soccer game while he was “playing up” on his older brothers team. He did need to do a lot of jumping as well as cutting. He is generally a midfielder/Forward. Well experienced player and “soccer is his life“.

My initial thoughts were something like a gastroc dysfunction or a Baker’s cyst. On examination, no masses or definitive swelling noted behind either knee. He did have tenderness to moderate degree over the right plantaris and tenderness as well as 4/5 weakness of the left popliteus. There was a loss of long axis extension of the talo crural articulations bilaterally with the loss of lateral bending to the right and left at L2-L3.

If you think about the mechanics of the right footed kicker (and try this while kicking a soccer ball yourself) it would be approximately as follows: left foot would be planted near the ball and the tibia/femur complex would be internally rotating well the foot is pronating and the popliteus would be eccentrically contracting to slow the rotation of the femur and the tibia. The right foot will be coming through and plantarflexion after a push off from the ball of the foot firing the triceps surae and plantaris complexes. He would be “launching“ off of the right foot and landing on his left just prior to the kick, causing a sudden demand on the plantar flexors; with the plantaris being the weak link. As the kicking leg follows through, the femur of the stance phase leg needs to externally rotate (along with the tibia) at a faster rate than the tibia (otherwise you could injure the meniscus) the popliteus would be contracting concentrically. A cleat, because it increases the coefficient of friction with the ground would keep the foot on the ground solidly planted and The burden of stress would go to the muscles which would be extremely routine leg and close chain which would include the semimembranosus/tendinosis  complex as well as the vastus medialis and possibly gracilis and short adductor, along with the popliteus.

I have to say and all of my years of practice I’ve never seen this combination type of injury before involving these two muscles specifically and am wondering if anyone else has seen this?

Dr Ivo Waerlop, one of The Gait Guys

#footproblem #gait #thegaitguys #soccerinjury #bilateralkneepain #popliteus #plantaris

image credit: https://commons.wikimedia.org/wiki/File:Slide2ACCA.JPG

image credit: https://commons.wikimedia.org/wiki/File:Slide2ACCA.JPG

Making a list and checking it twice…  
 So you or someone you are treating/coaching/ rehabbing, etc has muscle weakness, either perceived by them or noted by you, by observation or muscle testing. Have you stopped to think what might be causing the weakness? 
 Cross sectional area is directly proportional to strength. With strength, we are talking predominantly about Type II muscle (remember, Type I is predominantly endurance muscle, due to differing histological structure).    Type II muscle fibers are larger, have fewer capillaries, less myoglobin, fewer mitochiondra . They obtain most of their energy by anaerobic glycolysis, rather than aerobic respiration    (ie the Krebs cycle).    All muscles are made of a mixture of Type I and Type II fibers, but most muscles tend to have a predominance of one over the other. Here we are referring to strength. 
 There are many causes of muscle weakness. Here are a few: 
  Injury to the muscle 
 Injury to the joint the muscle crosses 
 Stretch weakness 
 Tight weakness 
 Neurogenic weakness 
 Myopathic weakness 
 Reflexogenic weakness 
 And the list goes on… 
  The 1 st  one on the list is an easy one to understand. If you break the machine, it doesn’t work. Torn contractile proteins with leaky sarcoplasmic reticulum (calcium reservoirs) do not allow for efficient contractions. 
 The second on the list is a bit more complex. 
 We remember that that the joint capsules are blessed with four types of mechanoreceptors, aptly named Type I, II, III, and IV, which when stimulated physically, chemically, or thermally apprise the nervous system of the forces acting on that joint as well as its position in space. For a great video review of mechanoreceptors, click  here  
 Joint pathology or inflammation will often cause distention of its capsule. The effect of the resulting joint effusion on the actions of the muscles crossing that joint have been examined extensively in the literature. Let’s look at one of the studies and its implications. 
  Reflex Actions of Knee Joint Afferents During Contraction of the Human Quadriceps  
  Iles JF, Stokes M, Young A: Clinical Physiology (10) 1990: 489-500  

 In this paper, the authors infuse hypotonic saline into the knees of eight asymptomatic individuals (including one of the authors) using a 16 gauge needle (ouch!) and studied its effects on the H reflexes and muscle recruitment. An H reflex is like performing a tendon jerk reflex (the  involuntary contraction  you would check with a neurological hammer) using an electrical stimulus. The onset time (also called the latency) and its amplitude are recorded. Muscle recruitment is the  voluntary contraction  of that muscle, measured with electromyography (EMG) by having an electrode either over (surface EMG) or within (needle EMG) the muscle and examining how hard the muscle is working based on the amplitude and frequency of the response. 
 First of all, no one in the study experienced any pain (hmmm, not sure about that) , only the sensation of pressure in their knees (which was considered activation of  only  the proprioceptors of the joint). The authors found that   any   pressure increase within the joint capsule depressed the H reflex and inhibited the action of the quadriceps. They hypothesize that this may contribute to pathological weakness after joint injury. 
 So how does all this apply to us? 
 As we all know, lots of patients have joint dysfunction. Joint dysfunction leads to cartilage irritation, which leads to joint effusion. This will inhibit the muscles that cross the joint. This causes the person to become unable to stabilize that joint and develop a compensation pattern. Next the stress is transferred to the connective tissue structures surrounding the joint which, if the force is sufficient, will fail. Now we have a sprain and some of the protective reflexes can take over. Abnormal forces can now be translated to the cartilage. This, if it goes on long enough,    can perpetuate degeneration, which causes further joint dysfunction. The cycle repeats and if someone doesn’t intervene and control the effects of inflammation, restore normal joint motion and rehabilitate the surrounding musculature, the patient’s condition will continue its downward spiral, becoming another statistic contributing to the tremendous economic and physical costs of an injury. 
  And that, my friends, is  one mechanism  as to how joint effusion disturbs the homeostasis of the musculature surrounding a joint.  
 In future posts, we will examine other causes of muscle weakness. For now, make a list of possible causes before assuming it is just injured or “turned off”. Compensations happen for a reason, and if you remove someone’s compensation pattern, you had better make sure you have another one up your sleeve and that their system is ready for a change. 
   The Gait Guys. Giving you the tools so you can be better. Period. 

Making a list and checking it twice…

So you or someone you are treating/coaching/ rehabbing, etc has muscle weakness, either perceived by them or noted by you, by observation or muscle testing. Have you stopped to think what might be causing the weakness?

Cross sectional area is directly proportional to strength. With strength, we are talking predominantly about Type II muscle (remember, Type I is predominantly endurance muscle, due to differing histological structure).  Type II muscle fibers are larger, have fewer capillaries, less myoglobin, fewer mitochiondra . They obtain most of their energy by anaerobic glycolysis, rather than aerobic respiration  (ie the Krebs cycle).  All muscles are made of a mixture of Type I and Type II fibers, but most muscles tend to have a predominance of one over the other. Here we are referring to strength.

There are many causes of muscle weakness. Here are a few:

  • Injury to the muscle
  • Injury to the joint the muscle crosses
  • Stretch weakness
  • Tight weakness
  • Neurogenic weakness
  • Myopathic weakness
  • Reflexogenic weakness
  • And the list goes on…

The 1st one on the list is an easy one to understand. If you break the machine, it doesn’t work. Torn contractile proteins with leaky sarcoplasmic reticulum (calcium reservoirs) do not allow for efficient contractions.

The second on the list is a bit more complex.

We remember that that the joint capsules are blessed with four types of mechanoreceptors, aptly named Type I, II, III, and IV, which when stimulated physically, chemically, or thermally apprise the nervous system of the forces acting on that joint as well as its position in space. For a great video review of mechanoreceptors, click here

Joint pathology or inflammation will often cause distention of its capsule. The effect of the resulting joint effusion on the actions of the muscles crossing that joint have been examined extensively in the literature. Let’s look at one of the studies and its implications.

Reflex Actions of Knee Joint Afferents During Contraction of the Human Quadriceps

Iles JF, Stokes M, Young A: Clinical Physiology (10) 1990: 489-500

In this paper, the authors infuse hypotonic saline into the knees of eight asymptomatic individuals (including one of the authors) using a 16 gauge needle (ouch!) and studied its effects on the H reflexes and muscle recruitment. An H reflex is like performing a tendon jerk reflex (the involuntary contraction you would check with a neurological hammer) using an electrical stimulus. The onset time (also called the latency) and its amplitude are recorded. Muscle recruitment is the voluntary contraction of that muscle, measured with electromyography (EMG) by having an electrode either over (surface EMG) or within (needle EMG) the muscle and examining how hard the muscle is working based on the amplitude and frequency of the response.

First of all, no one in the study experienced any pain (hmmm, not sure about that) , only the sensation of pressure in their knees (which was considered activation of only the proprioceptors of the joint). The authors found that any pressure increase within the joint capsule depressed the H reflex and inhibited the action of the quadriceps. They hypothesize that this may contribute to pathological weakness after joint injury.

So how does all this apply to us?

As we all know, lots of patients have joint dysfunction. Joint dysfunction leads to cartilage irritation, which leads to joint effusion. This will inhibit the muscles that cross the joint. This causes the person to become unable to stabilize that joint and develop a compensation pattern. Next the stress is transferred to the connective tissue structures surrounding the joint which, if the force is sufficient, will fail. Now we have a sprain and some of the protective reflexes can take over. Abnormal forces can now be translated to the cartilage. This, if it goes on long enough,  can perpetuate degeneration, which causes further joint dysfunction. The cycle repeats and if someone doesn’t intervene and control the effects of inflammation, restore normal joint motion and rehabilitate the surrounding musculature, the patient’s condition will continue its downward spiral, becoming another statistic contributing to the tremendous economic and physical costs of an injury.

And that, my friends, is one mechanism as to how joint effusion disturbs the homeostasis of the musculature surrounding a joint.

In future posts, we will examine other causes of muscle weakness. For now, make a list of possible causes before assuming it is just injured or “turned off”. Compensations happen for a reason, and if you remove someone’s compensation pattern, you had better make sure you have another one up your sleeve and that their system is ready for a change.

The Gait Guys. Giving you the tools so you can be better. Period.