Shoes and Pronation and Injuries

Our brief (very) thoughts on the topic in Triathlete.com. We do not do much of this stuff anymore, our thoughts get so “cooked down” that they often lose context. But thankfully the main principle was conveyed pretty well here, albeit not in entirety.

We were asked about this topic many moons ago. We did not know this was published in January, until a patient brought it to our attention this week.

http://triathlon.competitor.com/2015/01/training/pronation-blame-injuries_111767

Fascia Science

So you talk about fascia and adhesion and scar tissue with your clients, do you?
Glad someone finally said it. Kudos.
Hope this will foster good debate. Careful you do not get stuck on your loyalty to a method or guru.

http://www.greglehman.ca/2012/10/26/fascia-science-stretching-the-relevance-of-the-gluteus-maximus-and-latissimus-dorsi-sling/

Beware of research data

Be aware of what you read.
We have had many people over the years criticize some of the articles we put up….“hey, the N on this study is 6 ! That isn’t a reliable study” etc.
As we have said many times, you can pick apart many studies. Few are comprehensive, many just look at a small piece, and as our link today eludes to, some are frauds and listed from “pay-for-play” publications. Some however are just so flawed that publication should never have occurred.
However, just because you have a problem with an article does necessarily mean to throw the baby out with the bath water. Good or bad, most valid articles have something good or bad to learn from. Sometimes they spark ideas in our minds, sometime they encourage thought, change or avoidance. This is the value of a valid journal article to us, the bigger picture, not because the study only looked at one aspect of a theory or hypothesis.

Here is an article that is raising Cane in the nutrition world and it sort of highlights some problems.

“Bohannon, a science journalist who also has a Ph.D., lays out how he carried out an elaborate hoax to expose just how easily bad nutrition science gets disseminated in the mainstream media. "You have to know how to read a scientific paper — and actually bother to do it,” he writes. For starters, as Bohannon explains in great detail, the study design itself was flawed — it had too few subjects, and the research measured too many factors, making it likelier that some random factor would appear to have statistical significance.

http://www.npr.org/sections/thesalt/2015/05/28/410313446/why-a-journalist-scammed-the-media-into-spreading-bad-chocolate-science

The cross over gait and achilles pathologies.

From our post earlier today:

Part 2: 

Considered another way, from the top down this time, if at the moment of heel contact the gmedius is delayed (as suggested in the study below from achilles pain), the pelvis is likely to drift laterally and this could cause a reactive inversion strategy of the rearfoot, and maybe even forefoot as well, as an instinctive measure to try and draw support beneath the laterally drifting body mass center of gravity. (This in essence sets up the “cross over gait” deployment strategy we have talked about here for years now).This too could cause a change in load to the achilles mechanism, resulting in tendonopathy thus putting one into a vicious cycle of achilles causing glute and then glute perpetuating altered strike and thus abnormal achilles loads . This is also a major cause of ankle inversion sprains, so be extra aware of this pattern. We see this all the time in practice, we hope you do as well. IF you haven’t already, If you wish to dive deeper, goto our blogwww.thegaitguys.tumblr.com and type in Cross Over Gait and it will get you going.
* Remember this, if you are spending time moving sideways, you are taking from time moving forwards, in the allotted amount of time given for the stance phase of gait. Yet, you will still move forwards, so one way around this is a premature heel rise (ie. speed up certain mechanical events) via premature plantarflexion mechanism loading (calf-achilles complex). Remember to also look for all the other reasons for premature heel rise (ie. loss of ankle rocker etc).

Franettovich Smith MM1, Honeywill C, Wyndow N, Crossley KM, Creaby MW. : Neuromotor control of gluteal muscles in runners with achilles tendinopathy.
Med Sci Sports Exerc. 2014 Mar;46(3):594-9.

______________

Part 1

The mighty Gluteus Medius, in all its glory!

Perhaps the delayed action of the gluteus medius allows an adductory moment of the pelvis, moving the center of gravity medially. This could conceivably place additional stress on the achilles tendon (via the lateral gastroc) to create more eversion of the foot from midstance onward.

“The results of the study demonstrate altered neuromuscular control of the GMED and GMED in runners with Achilles Tendonitis. During running, GMED typically activates before heel strike so as to stabilize the hip and the pelvis. In runners with Achilles Tendonitis, GMED is activated with a delay, which consequently might affect the kinematics of knee and ankle resulting in rear foot inversion. Similarly, GMAX is activated with a delay and for a shorter duration in runners with Achilles Tendonitis. GMAX is the primary hip extensor and via a kinetic chain, a decreased hip extension moment might be compensated by an increased ankle plantarflexion moment which could potentially increase the load on the Achilles tendon.”

Franettovich Smith MM1, Honeywill C, Wyndow N, Crossley KM, Creaby MW. : Neuromotor control of gluteal muscles in runners with achilles tendinopathy.
Med Sci Sports Exerc. 2014 Mar;46(3):594-9.

Post stroke spatiotemporal gait asymmetries.

This could be translated into your non-stroke patients gait. Making changes in their gait must be specific, accurate (what they need, not changes that you are seeing which you do not like), and consciously engrained through repetition. As with most things, awareness is the first step toward change. And making changes based on what you see is just asking them to create a new pattern on what was likely their compensation, not their problem. Never change what you see in someones gait without a complete physical examination first, what you see is how they are moving with their presenting problem(s).

“Asymmetry magnitudes need to exceed usual overground levels to reach conscious awareness. Therefore, it is proposed that the spatiotemporal asymmetry that is specific to each participant may need to be augmented beyond what he or she usually walks with in order to promote awareness of asymmetric gait patterns for long-term correction and learning.”
“Following stroke, spatiotemporal gait asymmetries persist into the chronic phases, despite the neuromuscular capacity to produce symmetric walking patterns. This persistence of gait asymmetry may be due to deficits in perception, as the newly established asymmetric gait pattern is perceived as normal.”

http://ptjournal.apta.org/…/2015/04/30/ptj.20140482.abstract

Walking meditation

A different perspective on walking.
When we give our gait retraining homework to clients, we ask that it is mindful and that each step is focused on the changes we have recommended. We ask that they notice the local changes and eventually the global manifestations of these gait alterations. This is key to making changes, and as this piece eludes to……there is something deeper cerebrally going on that can change other deeper aspects of your life.

How to Walk is the fourth title in Parallax’s popular Mindfulness Essentials Series of how-to titles by Zen Master Thich Nhat Hanh, introducing beginners and reminding seasoned practitioners of the essentials of mindfulness practice. Slow, concentrated walking while focusing on in- and out-breaths allows for a unique opportunity to be in the present. - See more at: 

http://www.parallax.org/how-to-walk-thich-nhat-hanh-mindfulness-essentials/

Isometrics for patellar tendonitis?

We are familiar with different modes of exercise: isometric, isotonic and isokinetic. Isometric exercises have a physiological overflow of 10 degrees on each side of the point of application (ie; to do the exercise at 20 degrees flexion, and you have strength gains from 10 to 30 degrees); isotonics and isokinetics, 15 degrees. Taking advantage of physiological overflow often allows us to bypass painful ranges of motion and still strengthen in that range of motion. 

In this study, they looked at immediate and 45 minute later pain reduction (not function) comparing isometric (max voluntary quadricep contraction) and isotonic (single leg decline squat) exercises. They also looked at cortical inhibition (via the cortico spinal tract) as a result of the exercises. 

Here is what they found: “A single resistance training bout of isometric contractions reduced tendon pain immediately for at least 45 min postintervention and increased MVIC. The reduction in pain was paralleled by a reduction in cortical inhibition, providing insight into potential mechanisms. Isometric contractions can be completed without pain for people with PT. The clinical implications are that isometric muscle contractions may be used to reduce pain in people with PT without a reduction in muscle strength.” These same results were not seen with the isotonic exercise. 

Did the decrease in pain result in the decrease in cortical inhibition (muscle contraction is inhibited across an inflamed joint: Rice, McNair 2010; Iles, Stokes 1987)? Was it a play on post isometric inhibition (most likely not, since this usually only lasts seconds to minutes post contraction) ? Or is there another mechanism at play here? There has been one other paper we found here, that shows cortical inhibition of quadriceps post isometric exercise. Time will tell. In the meantime, start using those multiple angle isometrics!

The Gait Guys

Rio E, Kidgell D, Purdam C, Gaida J, Moseley GL, Pearce AJ, Cook J.Isometric exercise induces analgesia and reduces inhibition in patellar tendinopathy Br J Sports Med. 2015 May 15. pii: bjsports-2014-094386. doi: 10.1136/bjsports-2014-094386. [Epub ahead of print]

http://www.anatomy-physiotherapy.com/28-systems/musculoskeletal/lower-extremity/knee/1163-isometric-exercises-in-patellar-tendinopathy

The mighty Gluteus Medius, in all its glory!

Perhaps the delayed action of the gluteus medius allows an adductory moment of the pelvis, moving the center of gravity medially. This could conceivably place additional stress on the achilles tendon  (via the lateral gastroc) to create more eversion of the foot from midstance on

“The results of the study demonstrate altered neuromuscular control of the GMED and GMED in runners with Achilles Tendonitis. During running, GMED typically activates before heel strike so as to stabilize the hip and the pelvis. In runners with Achilles Tendonitis, GMED is activated with a delay, which consequently might affect the kinematics of knee and ankle resulting in rear foot inversion. Similarly, GMAX is activated with a delay and for a shorter duration in runners with Achilles Tendonitis. GMAX is the primary hip extensor and via a kinetic chain, a decreased hip extension moment might be compensated by an increased ankle plantarflexion moment which could potentially increase the load on the Achilles tendon.”

Franettovich Smith MM1, Honeywill C, Wyndow N, Crossley KM, Creaby MW. : Neuromotor control of gluteal muscles in runners with achilles tendinopathy.
Med Sci Sports Exerc. 2014 Mar;46(3):594-9.

The Mighty Interossei

By request of one of our readers (Thank you Richard S), we were asked to “dig up” some information about the interossei. After scouring the literature, we turned up an interesting paper, talking about their anatomy. 

Of interesting note, the paper found extensive connections of the musculature with the surrounding fascia (talk about myofascial meridians!) as well as a fairly consistent slip of the peroneus longus which contributes to the 1st dorsal interossei. This is important considering the peroneus fires from midstance on, as do the interossei (and other foot intrinsics). Perhaps (since as the fore foot is extending in late midstance and pre swing) it assists in descending the head of the 1st metatarsal and resisting extension (contracting eccentrically) of the metatarsal phalangeal joints, helping to maintain stability of the fore foot for push off. 

“The extensive connections among the interossei indicate that they could be important stabilisers of the foot during those times when rigidity is required. The pull of the interossei is transformed across the tarsometatarsal joints by means of their attachment to the ligamentous meshwork. Thus they will act upon the tarsometatarsal joints. Crossing those joints on their plantar aspect, the interossei are well placed to assist in resisting extension. Even though their close attachment proximal to the joints creates a short lever arm and therefore relative inefficiency as flexors when weight is borne on the ball of the foot (MacConaill, 1949), the large mass of the combined interossei probably indicates that they do have a significant role in resisting extension at these joints. Also, the shapes of the tarsometatarsal joint surfaces restrict angular motion.”

Definitely a good read and available FREE full text online here

PAUL J. KALINt AND BRUCE ELLIOT HIRSCH: The origins and function of the interosseous muscles of the foot  J. Anat. (1987), 152, pp. 83-91 

Abdominal Activity and Gait

We came across this cool study today, after a well educated patient asked about abdominal activity during gait.

Here is the bottom line:
low level activity in the rectus abdominis and external oblique throughout the gait cycle, more concentrated activity of the internal oblique at initial contact/loading response (heel strike).

This makes sense, since the external oblique occupies more real estate and has a larger cross sectional area; it most likely has a role in stabilization both in rotational like emoticon planes as well as the saggital plane (Z). Perhaps the action of the internal oblique at initial contact is to assist in external rotation of the pelvis on the stance phase leg, as the the opposite leg goes into swing?

“Cluster analysis identified two patterns of activity for the internal oblique, external oblique and rectus abdominis muscles. In the lumbar erector spinae, three patterns of activity were observed. In most instances, the patterns observed for each muscle differed in the magnitude of the activation levels. In rectus abdominis and external oblique muscles, the majority of subjects had low levels of activity (<5.0% of a maximum voluntary contraction) that were relatively constant throughout the stride cycle. In the internal oblique and the erector spinae muscles, more distinct bursts of activity were observed, most often close to foot-strike. The different algorithms used for the cluster analysis yielded similar results and a discriminant function analysis provided further evidence to support the patterns observed”

Clin Biomech (Bristol, Avon). 2002 Mar;17(3):177-84.
Abdominal and erector spinae muscle activity during gait: the use of cluster analysis to identify patterns of activity.
White SG1, McNair PJ.

Forefoot Varus Anyone?

Forefoot varus appears to move the center of gravity medially while walking. Nothing earthshaking here, but nice to see the support of the literature.

“The most medial CoP of the row and CoP% detected increased medial CoP deviation in FV ≥ 8°, and may be applied to other clinical conditions where rearfoot angle and CoP of the array after initial heel contact cannot detect significant differences.”

We will be talking about foot types this week on onlinece.com; Wednesday 8 EST, 7 CST, 6MST, 5 PST Biomechanics 314. Hope to see you there!

J Formos Med Assoc. 2015 May 5. pii: S0929-6646(15)00132-1. doi: 10.1016/j.jfma.2015.03.004. [Epub ahead of print]
Analysis of medial deviation of center of pressure after initial heel contact in forefoot varus.

picture from: http://forums.teamestrogen.com/showthread.php?t=46901

Clinical tidbit:

Heel pain in kids and adolescents? Have you considered Sever’s disease?

Apophysitis of the calcaneal apophysis is the most common cause of heel pain in adloscents and accounts for 8% of all pediatric overuse injuries! An apophysitis occurs (an injury involving a “pulling away” of bone from the tendons attachment site) because the strength of the tendon exceeds the strength of attachment of the tendon to the bone. It is most common in activites llike running, jumping and plantar flexion.

Gillespie H. Osteochondroses and apophyseal injuries of the foot in the young athlete. Curr Sports Med Rep 2010;9(5):265-268.

Wilson JC, Rodenburg RE. Apophysitis of the lower extremities. Contemp Pediatr 2011;28(6):38-46.

Ahh yes, the lumbricals. 

One of our favorite muscles. And here it is in a recent paper! This one is for all you fellow foot geeks : )

Perhaps the FDL (which fires slightly earlier than the FHL) and FHL (which fires slightly later and longer) at loading response, slowing pronation and setting the stage for lumbrical function from midstance to terminal stance/preswing (flexion at the metatarsal phalangeal joint (it would have to be eccentric, if you think about this from a closed chain perspective) and extension (actually compression) of the proximal interphalangeal joints.

“The first lumbrical arose as two muscle bellies from both the tendon of the FDL and the tendinous slip of the FHL in 83.3 %, and as one muscle belly from the tendon of the FDL or the tendinous slip of the FHL in 16.7 %. These two muscle bellies subsequently merged to form the muscle belly of the first lumbrical. The second lumbrical arose from the tendinous slips of the FHL for the second and third toes as well as the tendon of the FDL in all specimens. The third lumbrical arose from the tendinous slips of the FHL for the third and fourth toes in 69.7 %, and the fourth lumbrical arose from the tendinous slip of the FHL for the fourth toe in 18.2 %. Some deep muscle fibers of the fourth lumbrical arose from the tendinous slip of the FHL for the second toe in 4.5 %, for the third toe in 28.8 %, and for the fourth toe in 15.2 %.”

Hur MS1, Kim JH, Gil YC, Kim HJ, Lee KS. New insights into the origin of the lumbrical muscles of the foot: tendinous slip of the flexor hallucis longus muscle. Surg Radiol Anat. 2015 May 12. [Epub ahead of print]

Prior hamstring injuries

Previous hamstring injury is associated with altered biceps femoris associated muscle activity and potentially injurious kinematics.

“Previously injured athletes demonstrated significantly reduced biceps femoris muscle activation ratios with respect to ipsilateral gluteus maximus, ipsilateral erector spinae, ipsilateral external oblique, and contralateral rectus femoris in the late swing phase. We also detected sagittal asymmetry in hip flexion, pelvic tilt, and medial rotation of the knee effectively putting the hamstrings in a lengthened position just before heel strike.”
http://onlinelibrary.wiley.com/d…/10.1111/sms.12464/abstract

Foot “core” anyone?

And a good time was had by all. Day 1 of the event in Vancouver. Lots of info and a bonus exercise session. Thanks to all who attended and looking forward to another great day tomorrow!

We spent a great deal of time talking about muscular firing sequences and the reasoning as to why things fire when.

Take a look at the picture and focus on the tib posterior, flexor digitorum longus, and flexor hallucis longus. They fire from loading response and fire through terminal stance. Up to midstance, they act eccentrically to slow pronation and after midstance, they fire concentrically to assist in supination. Note the sequence starts with the tib posterior (more proximal attachments in the foot) and ends with the flexor hallucis longus, more distal attachements (because in “ideal” gait, the hallux is the last to leave the party (or the ground, in this case)). Stability is a priority, so the central or “core” of the foot needs to fire before adding on peripheral (appendicular) muscles. Remember the foot intrinsics fire from midstance to pre swing, further stabilizing the foot “core”

The Gait Guys

Attempting to regain a level playing ground for your foot.

“Remember, we were born with both our rearfoot and forefoot designed to engage on the same plane (the flat ground). We were not born with the heel raised higher than the forefoot. And, the foot’s many anatomically congruent joint surfaces, their associated ligaments, the lines of tendon pull and all the large and small joint movements and orchestrations with each other are all predicated on this principle of a rearfoot and forefoot on the same plane. This is how our feet were designed from the start.  This is why I like shoes closer to zero drop, when possible, because I know that we are getting closer to enabling the anatomy as it was designed. This is not always possible, feasible, logical or reasonable depending on the problematic clinical presentation and there is plenty of research to challenge this thinking, yet plenty to support is as well. The question is, can you get back to this point after years of footwear compensating ? Or have your feet just changed too much, new acquired bony and joint changes that have too many miles on the new changes ? Perhaps you have spent your first 20-50 years in shoes with heeled shoes of varying heel-ball offset. Maybe you can get back to flat ground, maybe you cannot, but if you can, how long will it take? Months ? Years ?  It all makes sense to me, but does it make sense for your feet and your body biomechanics after all these years ? Time will tell.” -Dr. Allen

Fundamental foot skills everyone should have, subconsciously. This video shows a skill you must own for good foot mechanics. It needs to be present in standing, walking, squatting, jumping and the like. It is the normal baseline infrastructure that you must have every step, every moment of every day. 

Is your foot arch weak ? Still stuffing orthotics and stability shoes up under that falling infrastructure ? Try rebuilding a simple skill first, one that uses the intrinsic anatomy to  help pull the arch up.  If your foot is still flexible, you can likely re-earn much of the lost skills, such as this one. This is a fundamental first piece of our foot, lower limb and gait restoration program. We start here to be sure this skill is present, then add endurance work on it and then eventually strength and gait progressions. This is where it starts for us gang. 

Shawn and Ivo, the gait guys

More muscle madness (or weakness, as the case may be)

In the last post (missed it? click here) , we discussed 3 causes of muscle weakness: local, segmental and cortical. In that post, we emphasized LOCAL causes of muscle weakness, determining that many of these causes related to direct injury, disease processes or neuromuscular endplate disorders.

This post will look at segmental causes, which as you have probably guessed, are at the spinal cord level. These are usually “electrical” problems, though in uncommon cases (syrinx, ependyoma, dermoid tumors) thay can be due to pathological processes. 

We need to understand that the spinal cord is composed of either tracts or nucleii, that’s pretty much it. The tracts are largely on the outside of the cord. Remember that they are the axons of nerves. Since they are myelinated (insulated), they are white in appearence. They have names like the spinocerebellar tracts, dorsal columns, reticulospinal tracts and corticospinal tracts, just to name a few. The nucleii are largely in the central part of the cord, organized in an “H” pattern that is divided up into layers called lamina. They are unmyelinated, so they are grey in appearance. Interspersed with these nucleii are perhaps one of the most important contributors to muscle weakness, the “interneurons” or “interneuronal pool”.

Remember, as impulses travel down from the cortex to control volitional (voluntary)movement, they end here in the internuncial pool and land on, you guessed it, interneurons. To this end, we need to remember that interneurons are 30X more numerous than any of the other cells in the central part of the cord. When a message is on its way down from the cortex, or heading up to it, most of the time, it interacts with an interneuron. In turn, interneurons can be excitatory or inhibitory. 

Something you should know about neurons, is that they are all or none. They either fire or they don’t. There is no in between. Same for interneurons. Depending on what they are connected to, the muscles (or autonomics, or other 2nd and 3rd order neurons) fire…or they don’t.

There are 2 types of motor neurons that go to muscle: alpha and gamma. Alpha motor neurons go to “extrafusal” muscle, or muscle we can control voluntarily. Gamma motor neurons go to “intrafusal” muscle, or muscle spindles, which monitor the length and rate of change of length of a muscle.

As you probably guessed, these motor neurons can be either activated directly (few) or through interneurons (many). These motor neurons connect with sensory neurons that monitor things like length, rate of change of length and tension in muscles. These modalities are subserved by receptors you have heard of: muscle spindles and golgi tendon organs. The alpha and gamma motor neurons also interact with axons of neurons that are descending from higher areas of the brain, like the cortex, cerebellum, vestibular nucleus, just to name a few.

It is the interplay of all these inputs and outputs, often referred to as the “central integrated state”, that ultimately determines whether a muscle fires or not, and thus if it is “weak” or “strong”. If excitation wins, then the nerve fires and the muscle contracts; if inhibition wins, then it does not. 

What are all the inputs and outputs? Only all the sensory and motor (this includes the autonomics ie sympathetic and parasympathetic) information arriving there from the periphery and central nervous system! Quite a lot!

Segmental causes, just another reason a muscle may test week

Ivo and Shawn: The Gait Guys

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.

http://www.mikereinold.com/2009/05/10-principles-of-patellofemoral.html

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…

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