Medial or lateral ankle swelling. Not a unicorn, but perhaps close. 

Photo: note the enlargement of the soft tissue in the left medial achilles area.

Many times over the last 5 years we have written about the concept that you have to know something exists to even make it a clinical consideration when trying to troubleshoot a clients pain or problem. Without knowing something even exists, you will move onto another diagnostic assumption and perhaps be treating the wrong problem.  This is a big problem in medicine because there is no way any of us knows everything. But this is why we all read, we study, we ask questions and we learn from our mistakes and depend on lateral and higher pay-grade referrals.  

Look at the photos above. Do you or your client have a posterior mass or swelling along side the achilles, medially or laterally ? Are you a rare bipedal mammal or do you have a lipoma, hemagioma or even sarcoma ?  Perhaps it is a swollen achilles ? Are there nodular densities in the achilles tendon proper that might suggest micro tears ? Are the regional busae swollen ? Those are all logical first steps, but maybe it is just a rarity, a more common unicorn of lower limb anomalies (10% incidence), the “accessory soleus”.

When an accessory soleus muscle is present a soft-tissue mass appears bulging medially between the distal part of the tibia and the Achilles tendon. This apparent “swelling”, may be entirely symptom free because it is merely an anatomic variant.  However, variants can become a problem when they impair stability or mobility or when they become irritated because of the same issues elsewhere.  This muscle has its own individual tendon slip onto the calcaneus anteromedial to the Achilles insertion.  This entity is not always painful or symptomatic but it can be expressive during exercise in some clients.  When they present clinically symptomatic one must rule out pathomechanics of the foot, ankle or lower kinetic chain.  The appearance of the assessory soleus is easily diagnostic on CT and MRI imaging. Some sources recommend fasciotomy or excision of the accessory muscle, clearly radical initial measures, but most of the time they can be quieted by resolving the pathomechanics that have allowed this previously quite clinical entity to become symptomatic. If the problem is just recently symptomatic, it is likely not the problem, rather the environment (workout changes, shoe changes, tissue length-tension relationship changes, mobility or stability changes etc) has changed and put a demand on the area and created once quiet tissues to complain.

First one must rule out the nasties, as we eluded to earlier (lipoma, hemagioma, synovial sarcoma etc) and then rule out the complainers (busae, tendonopathies etc) and then look at mobility and stability deficits/challenges. Once all of the more likely suspects have been ruled out, it is time for considering unicorns.

Here are some thoughts. On heel rise does the soft tissue mass become firm as in a muscular contraction would become firm ? After all, it is a soleus component and can act as an ankle plantarflexor of the ankle. Or it is merely firm on forced dorsiflexion because the achilles is drawn firm and tight against the posterior tibia thus medially displacing the soft tissue into a smaller more compacted area? Is the area painful on running ? Jumping? Starts and stops ? Only painful during rest, going up stairs, down stairs, only biking, swimming ? One can see that an understanding the mechanics of an area and how to challenge that area to your diagnostic advantage can help you tease out many of the considerations above.  In this day and age, we always have imaging to fall back on, but remember, imaging is a static picture in a moment of time in an unloaded unfunctional posturing. You will treat your client and their problem, not the imaging. If they in fact do turn out to have an accessory soleus that is inflamed on imaging, you still have to figure out why it has suddenly become cranky and painful. The bottom line is that many people with a painful accessory soleus are coming to you because something they have done, or are doing, or are  compensating around is causing a change in mechanics that is bothering the tissue.  This is where your knowledge of the kinetic chain and foot types, shoe types (see our National Shoe Fit program review here) and gait biomechanics can be invaluable.  Figuring out these issues should be your first line of intervention, and then confirmation on imaging can truly be valuable. 

The accessory soleus, is a more common entity in primates. Is this further proof we used to have tails and swing from trees ? Maybe not, but it is still fun to think about though. 

Shawn and Ivo, the gait guys

Can the VMO be selectively activated?

They have a common nerve innervation, so many studies say no. Perhaps altering internal/external orientation of the lower extremity (1) or joint angles (2) may play a role. Of course, it also depends on how you are measuring (3). Intramuscular seems to be most accurate!

In the Link Below, section 4, is a nice, brief review of the literature. Thanks to Daithi Grey for the inspiration to put this up!

1. J Strength Cond Res. 2014 Sep;28(9):2536-45. doi: 10.1519/JSC.0000000000000582.
Range of motion and leg rotation affect electromyography activation levels of the superficial quadriceps muscles during leg extension.Signorile JF1, Lew KM, Stoutenberg M, Pluchino A, Lewis JE, Gao J.

2. Phys Ther Sport. 2013 Feb;14(1):44-9. doi: 10.1016/j.ptsp.2012.02.006. Epub 2012 Jun 26.
Muscle activation of vastus medialis obliquus and vastus lateralis during a dynamic leg press exercise with and without isometric hip adduction. Peng HT1, Kernozek TW, Song CY.

3. J Electromyogr Kinesiol. 2013 Apr;23(2):443-7. doi: 10.1016/j.jelekin.2012.10.003. Epub 2012 Nov 8.
The VMO:VL activation ratio while squatting with hip adduction is influenced by the choice of recording electrode. Wong YM1, Straub RK, Powers CM.

10 Principles of Patellofemoral Rehabilitation – Mike Reinold

“Emphasize the QuadricepsThe next principle of patellofemoral rehabilitation is to strengthen the knee extensor musculature. Some authors have recommended emphasis on enhancing the activation of the VMO in patellofemoral patients based on reports of isolated VMO insufficiency and asynchronous neuromuscular timing between the VMO and VL.While the literature offers conflicted reports on selective recruitment and neuromuscular timing of the vasti musculature, the VMO may have a greater biomechanical effect on medial stabilization of the patella than knee extension due to the angle of pull of the muscle fibers at approximately 50-55 degrees.  Wilk et al(JOSPT 1998) suggest that the VMO should only be emphasized if the angle of insertion of the VMO on the patella is in a position in which it may offer a certain degree of dynamic or active lateral stabilization.  As you can see by the figure, if the fibers are not aligned in a position to assist with patellar stabilization, VMO training will likely not be effective.  This orientation of the muscle fibers will differ from patient to patient and can be visualized.Several interventions and exercise modifications have been advocated to effectively increase the VMO:VL ratio, based mostly on anecdotal observations. These include hip adduction, internal tibial rotation, and patellar taping and bracing. Powers(JOSPT 1998) reports that isolation of VMO activation may not be possible during exercise, stating that several studies have shown that selective VMO function was not found during quadriceps strengthening exercises, exercises incorporating hip adduction, or exercises incorporating internal tibial rotation. Powers also states that although the literature offers varying support for VMO strengthening, successful clinical results have been found while utilizing this treatment approach.My belief is that quadriceps strengthening exercises should be incorporated into patellofemoral rehabilitation programs. Strength deficits of the quadriceps may lead to altered biomechanical properties of the patellofemoral and tibiofemoral joints. Any change in quadriceps force on the patella may modify the resultant force vector produced by the synergistic pull of the quadriceps and patellar tendons, thus altering contact location and pressure distribution of joint forces. Furthermore, the quadriceps musculature serves as a shock absorber during weightbearing and joint compression, any abnormal deviations in quadriceps strength may result in further strain on the patellofemoral and/or tibiofemoral joint.In reality, I believe that quadriceps strengthening is very important for patellofemoral rehabilitation, but many exercises designed to “enhance VMO” strength or activation may actually be disadvantageous to the joint.  Take for example the classic squeezing of the ball during closed kinetic chain exercises such as squatting and leg press.  This creates an IR and adduction moment at the hip that is now known to be detrimental to patellofemoral patients.  I would actually propose that we work on quadriceps strengthening without an adduction component and rather emphasize hip adbuction and external rotation.  This can be performed with the use of a piece of exercise band around the patient’s knees during these exercises. “

More on weak muscles. Just WHY are they weak? Know before you activate!

Dr Allen’s post last week on chronic ankle instability (click here for post) served as an inspiration for many of us. It brings to mind the many reasons muscles can become “weak”.

So why does a muscle become weak? We like to categorize the causes as follows:

  • local
  • segmental
  • long loop/cortical

Local causes include muscle injury and muscle pathologies, like muscular dystrophy and neuromuscular endplate disorders like myasthenia gravis. Segmental causes are largely due to reflexes which occur at the spinal cord level. Long loop and cortical causes ae due to an increased inhibition or lack of drive from higher centers, such as the motor cortex and cerebellum.

Lets examine local causes in more detail. To understand causes we must understand what makes a muscle contract.

Muscles are composed of many proteins, 2 of which are actin and myosin (see above). Actin has 2 forms, F (filamental) and G (globular) actin. Imagine 2 grapefruits side by side (G actin) held together in the middle by small filaments (F actin). Now imagine these another set immediately below, in a repeating pattern. These groups of 2 are held together at the sides by an additional protein called tropomyosin. This whole complex looks a little like train tracks. Along the strands of tropomyosin, at regular intervals is yet another protein called troponin. We like to think of troponin as a triangular shaped protein and each part of the triangle has a particular binding site: one for tropomyosin, one for actin and another for calcium ions.

Myosin is another component of muscle, that looks similar to a bunch of golf clubs. The head of the club will, under the right circumstances, interact with actin, the body (tail) of the club interacts with other myosin bodies.

Globular actin and myosin heads are like 2 teenagers and like to interact with one another. Normally, in a resting state, troponin protein covers the active site of myosin binding on G actin. In the presence of calcium, there is a change in shape of the troponin molecule, moving it off of the active site of actin, allowing myosin to bind there. When this happens, the head ratchets and muscle contraction occurs. In the presence of adequate fuel (ie ATP) the myosin head detaches from actin and “recocks”, ready for another contraction cycle (see 2nd picture above).

So where does the calcium come from? It is stored in areas of the muscle called the terminal cisterns. It is released when an action potential fires the peripheral nerve to the neuromuscular endplate of a muscle.

Can calcium be released any other way? Sure it can. How about if the terminal cisterns are damaged, from an injury to the muscle? How about if they are damaged from a disease process?

So, when calcium is released, no matter how it is released, muscles contract. If calcium is not released, then muscles do not contract.

From a local cause, If a muscle is weak, one of the following are usually causing the weakness:

  • there is physical damage to the muscle causing fewer of the working units of the muscle (called sarcomeres) contract

this is by far the most common, due to overuse or trauma

  • there is a problem with the connection of the nerve to the muscle

Disruption of nerve to muscle connections can be also be due to trauma or disease. Weakness that is becoming progressive and worsening, needs to be evaluated further and may be the signal for a progressive muscular or neurological disorder (muscular dystrophy, myasthenia gravis, Gullian Barre, etc)

  • there is insufficient neurotransmitter at the neuromuscular end plate to fire the muscle

this is usually due to a disease process

  • Insufficient calcium could theoretically hamper a muscles contraction, but since calcium is involved with nerve transmission as well, tetany (ie sustained contraction and spasm) would most likely occur due to other reasons that we will not explore at this juncture.

OK, so that sums up local causes. Look for a follow up post about segmental causes next…

We are: The Gait Guys

Last week we ran an archived piece named, “Just because a muscle tests weak doesn’t mean it  needs to be activated”.  Here is the link to that piece.

Today we present some more proof behind our stance on this topic. The referenced article below states in its Context: “An arthrogenic muscle response (AMR) of the soleus and peroneal muscles has been previously demonstrated in individuals with chronic ankle instability (CAI), but the presence of AMR in muscles acting on joints proximal to unstable ankles has not been previously explored.”

And here was their study’s conclusion: “Arthrogenic inhibition of the hamstrings muscles bilaterally and facilitation of the quadriceps muscle ipsilateral to the involved limb were noted in subjects with unilateral CAI. Motoneuron pool excitability appears to be altered in muscles that act on joints proximal to the ankle in those with unilateral CAI.”

This proves our thoughts on a deeper level.  Just because a muscle tests weak does not mean that this muscle is weak or “inactive” or needs  to be “activated”. It is a shame it is not as simple as finding something weak and “activating” it. As we eluded to, this is a far more complex system than that, there are complex feed forward and feedback loops that are mandated and regulated by local cord reflexes, pattern generators and complex cortical loops.  Putting a muscle “back on the grid” prior to activity merely because it tested weak may be putting your client at risk if you are not getting down to the bottom of the problem.  Taking the study mentioned here to a deeper level, finding out that your client has a weak hamstring or quad and negating the possible source of the problem down in an ankle could be devastating to an athlete if they are suddenly returned to aggressive activity immediately after being “activated”.  You may be over riding the central pattern generators, reflex responses and complex cortical loops arthrogenic responses, which could be neuro-protectively calculated. As this article mentioned, “motoneuron pool excitability appears to be altered in muscles that act on joints proximal to the ankle in those with unilateral CAI”.  This is a massively diffuse process going on constantly throughout the body, providing safe mobility and stability. It is not a random process and should not be intervened therapeutically on a random level. At the very least, it requires a patient history, clinical examination, gait evaluation and movement pattern assessment. Anything less is, well, your responsibility if poop hits the fan when they step on the field. 

Shawn and Ivo


J Athl Train. 2007 Jul-Sep; 42(3): 355–360.PMCID: PMC1978472Arthrogenic Muscle Response of the Quadriceps and Hamstrings With Chronic Ankle InstabilityEdward J Sedory, MEd, ATC, EMT,Eric D McVey, MEd, ATC,Kevin M Cross, MEd, ATC, PT,Christopher D Ingersoll, PhD, ATC, FACSM, and Jay Hertel, PhD, ATC, FACSM

“Neural circuits linking activity in anatomically segregated populations of neurons in subcortical structures and the neocortex throughout the human brain regulate complex behaviors such as walking, talking, language comprehension, and other cognitive functions associated with frontal lobes.” 1

We also found this interesting quote from Science Daily on this topic of complex sensory motor behaviors and on the varying information on central pattern generators.

ScienceDaily (June 3, 2012) — “A new finding that motor cortex is a dynamic pattern generator upends existing theory with broad implications for neuroscience.”

“Maybe it is actually easier to understand than we thought. A new paper presents some compelling evidence that the motor cortex, rather than being command central, is more like a part of the machine, sending rhythmic signals down the spinal cord to orchestrate movement.”

"The electrical signal that drives a given movement is therefore an amalgam — a summation — of the rhythms of all the motor neurons firing at a given moment.” This is of course monitored (and modified) by one of our best friends, the cerebellum. 2

The cortex is where movement begins and where it ends; from areas 4, 4s and 6 in the precentral gyrus of the brain’s frontal lobe, down the spinal cord and out to the muscle through the peripheral nerve.   It is also where the information from the body’s receptors feed back,  to give updates on where the body parts are in space (proprioception) and how they are doing functionally (comparing information about length, tension, etc).  It is about sensory and motor function.  Motor function is based on sensory input.  Good motor function is based on good sensory information. It is a subtle, beautiful, intricate symphony.  And when one part goes wrong, the whole system can be thrown off.  

Here is an example we sometimes use in our lectures and with our patients to make this point clear.  Imagine an orchestra playing Beethoven’s beautiful Ode to Joy, a choral symphony for orchestra.  Now imagine one of the musicians begins to play off key. In time, the musicians sitting around that musician who are most locally influenced by that off tune musician, soon become irritated and have troubles playing “in tune”. In time, if not rectified, the whole orchestra could be corrupted and being to take that lead as well.  Hard to believe, but it makes the point that all it takes is one piece not playing well to change the outcome. Similar analogy, all it takes is one weak muscle or one painful joint and the outcome is skewed away from the optimal outcome and in time local dysfunction and compensation becomes an all encompassing compensation. The body’s function and operation, when proper, is an orchestra and orchestration with each piece doing a local job with a more global contribution to the bigger job. When all pieces come together appropriately it creates a symphony of flawless, effortless movement as seen in the video above.

Shawn and Ivo, the gait guys


1. Front Syst Neurosci. 2014 Feb 13;8:16. eCollection 2014. Cognitive motor interactions of the basal ganglia in development .  Leisman G1, Braun-Benjamin O2, Melillo R3.

Simple Foot Exercises are effective!

Conclusion “These results suggest that the toe spread out (TSO) exercise can be recommended for preventing or correcting HV deformity at an early stage.”

We know and teach that foot exercises work. Here is a nice objective paper (click underlined for abstract) on two exercises we prescribe often.

Here is our variation of the TSO exercise we call the “Lift, Spread and Reach” exercise

Stand comfortably with your feet about shoulder width apart

Stand on your foot tripod with your toes extended. Concentrate on feeling pressure at the center of the calcaneus, the head of the 1st metatarsal and the head of the 5th metatarsal

Lift your toes as high as possible

Spread out (abduct) your toes as much as possible

Reach forward with your toes as far as possible

Place your toes back don on the ground as flat as possible.

repeat 10 X

You can augment the exercise with a rubber band around the toes to provide resistance after you can perform the exercise competently.

Happy exercising!

Ivo and Shawn

Kim MH1, Kwon OY, Kim SH, Jung DY.: Comparison of muscle activities of abductor hallucis and adductor hallucis between the short foot and toe-spread-out exercises in subjects with mild hallux valgus

J Back Musculoskelet Rehabil. 2013;26(2):163-8. doi: 10.3233/BMR-2012-00363.

Gait and any form of locomotion are highly complicated with many pieces necessary to achieve clean, smooth, coordinated motion.
Failure in only one piece of the puzzle can result in profound unhinging of the entire system because of the entangled nature of the feedback loops.
“ Proprioceptive feedback from extensor muscles during the stance phase ensures that the leg does not go into swing when loaded and that the magnitude of extensor activity is adequate for support. Proprioceptive feedback from flexor muscles towards the end of the stance phase facilitates the initiation of the swing phase of walking. Evidence that muscle afferent feedback also contributes to the magnitude and duration of flexor activity during the swing phase has been demonstrated recently. The regulation of the magnitude and duration of extensor and flexor activity during locomotion is mediated by monosynaptic, disynaptic, and polysynaptic muscle afferent pathways in the spinal cord. In addition to allowing for rapid adaptation in motor output during walking, afferent feedback from muscle proprioceptors is also involved in longer-term adaptations in response to changes in the biomechanical or neuromuscular properties of the walking system.” – Lam and Pearson
Neuroscientist. 2004 Jun;10(3):247-59. Cerebellar control of balance and locomotion. Morton SM1, Bastian AJ.