Podcast 151: Gait and neurology of movement, including, Tightness? shortness? What’s the difference? It's the Neurology.

Truths about Stretching, a case of sesamoiditis, plus exercised induced muscle damage and impaired motor learning, central fatigue, POSE and Chi running and injuries. This is a good one gang, do not miss it !

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doctorallen.co
summitchiroandrehab.com
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Our website is all you need to remember. Everything you want, need and wish for is right there on the site.
Interested in our stuff ? Want to buy some of our lectures or our National Shoe Fit program? Click here (thegaitguys.com or thegaitguys.tumblr.com) and you will come to our websites. In the tabs, you will find tabs for STORE, SEMINARS, BOOK etc. We also lecture every 3rd Wednesday of the month on onlineCE.com. We have an extensive catalogued library of our courses there, you can take them any time for a nominal fee (~$20).

Our podcast is on iTunes and just about every other podcast harbor site, just google "the gait guys podcast", you will find us.

Where to find us, the podcast Links:
Apple podcasts:
https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138?mt=2

Google Play:
https://play.google.com/music/m/Icdfyphojzy3drj2tsxaxuadiue?t=The_Gait_Guys_Podcast

Other links for today's show:

http://traffic.libsyn.com/thegaitguys/pod_151final.mp3

http://thegaitguys.libsyn.com/gait-and-neurology-of-movement-including-tightness-shortness-whats-the-difference-its-the-neurology

http://directory.libsyn.com/episode/index/id/11168369

Show notes and links:

We lose muscular Strength as we age.
Changes in supra-spinal activation play a significant role in the age-related changes in strength.
This motor system impairment can be improved by heavy resistance training
https://www.ncbi.nlm.nih.gov/pubmed/25940749

Age (Dordr). 2015 Jun;37(3):9784. doi: 10.1007/s11357-015-9784-y. Epub 2015 May 5.
Strength training-induced responses in older adults: attenuation of descending neural drive with age. Unhjem R1, Lundestad R, Fimland MS, Mosti MP, Wang E.

Osteoarthritis and running
https://journals.lww.com/acsm-csmr/Abstract/2019/06000/Running_Dose_and_Risk_of_Developing.5.aspx
Recent literature adds to a growing body of evidence suggesting that lower-dose running may be protective against the development of osteoarthritis, whereas higher-dose running may increase one's risk of developing lower-extremity osteoarthritis. However, running dose remains challenging to define, leading to difficulty in providing firm recommendations to patients regarding the degree of running which may be safe.

Can even experienced orthopaedic surgeons predict who will benefit from surgery when patients present with degenerative meniscal tears? A survey of 194 orthopaedic surgeons who made 3880 predictions
Non-surgical management is appropriate as first-line therapy in middle-aged patients with symptomatic non-obstructive meniscal tears.
https://bjsm.bmj.com/content/early/2019/08/12/bjsports-2019-100567

Sports Biomech. 2019 Jul 31:1-16. doi: 10.1080/14763141.2019.1624812. [Epub ahead of print]
Running biomechanics before and after Pose® method gait retraining in distance runners.
Wei RX1, Au IPH1, Lau FOY1, Zhang JH1, Chan ZYS1, MacPhail AJC1, Mangubat AL1, Pun G1, Cheung RTH1.

Pincer toe nails.

Screen Shot 2018-11-11 at 8.47.23 AM.png

Pincer Toe nails: You've seen them; did you know what they were and how they got that way? Or, did you dismiss them?

We think Hitomi’s hypothesis is correct. Here is why (this is paraphrased from our blog post on subungal hematomas and our revolutionary thinking on why they occur and it seems to fit well with pincer nail formation as well).

… when the skin is pulled at a differential rate over the distal phalange (from gripping of the toes rather than downward pressing through the toe pad) there will be a net lifting response of the nail from its bed as the skin is drawn forward of the backward drawn phalange (there is a NET movement of skin forward thus lifting the nail from its bedding). For an at-home example of this, put your hand AND fingers flat on a table top. Now activate JUST your distal long finger flexors so that only the tip of the fingers are in contact with the table top (there will be a small lifting of the fingers). There should be minimal flexion of the distal fingers at this point. Note the spreading and flattening of the nail. Now, without letting the finger tip-skin contact point move at all from the table, go ahead and increase your long flexor tone/pull fairly aggressively. You are in essence trying to pull the finger backward into flexion while leaving the skin pad in the same place on the table. Feel the pressure building under the distal tip of the finger nail as the skin is RELATIVELY drawn forward.] This is fat pad and skin being drawn forward (relative to the phalange bone being drawn backward) into the apex of the nail. Could this be magnifying the curvature of the nail and not offsetting the “automatic curving and shrinkage” function of the nail ? We think it is quite possible.

We have more to say on this topic, the above is just an excerpt of our blog post. More here, in the link below

https://thegaitguys.tumblr.com/post/127638788139/pincher-nails-who-knew-written-by-dr-shawn?fbclid=IwAR06ol516n9WF2Qh5TadlKd8esXrH5pVviycT_7QiMeScL0UJ3H9r1FF_OQ

Do you have dorsal (top) foot pain? Think you are tying your shoes too tightly?

Do you have dorsal (top) foot pain, at the peak of the arch? Think you are tying your shoes too tightly and that is the cause? Do you have pain over the dorsal or plantar mid foot on heel rise or jumping/landing or going up stairs ?

Just because you raise your heel and load the ball of the foot does not necessarily mean you have adequately plantarflexed the 1st metatarsal and loaded it soundly/stable with the medial tarsal bone. Heel rise, and thus loading onto the medial foot tripod, must be met with ample, stable, durable, 1st metatarsal plantarflexion and the associated medial tarsal bones. Also, without this, loading of the sesamoids properly cannot occur, and pain may ensue.

The first ray complex can be delicate in people who are symptomatic. In some people who do not have a good tibialis posterior-peroneus sling mechanism working harmoniously, in conjunction with a competent arch tripod complex to achieve a compentent arch complex (ie, EDL, EHL, tib anterior and some of the other foot intrinsics) this tarsometatarsal interval can become painful and instead of the 1st ray complex being stable and plantarflexing as the heel departs and the 1st ray begins taking load, it may not do so in a stable plantarflexed posturing. In some people it can momentarily dorsiflex as the arch subtly collapses (when it should be stable and supinated in heel rise).

"Subtle hypermobility of the first tarsometatarsal joint can occur concomitantly with other pathologies and may be difficult to diagnose. Peroneus Longus muscle might influence stability of this joint. Collapse of the medial longitudinal arch is common in flatfoot deformity and the muscle might also play a role in correcting Meary's angle."-Duallert et al

Soon, I hope to show you a video of how to watch for this problem, how to train it properly, how we do it in my office.
Dr. Allen

https://www.ncbi.nlm.nih.gov/pubmed/27015031

Clin Biomech (Bristol, Avon). 2016 May;34:7-11. doi: 10.1016/j.clinbiomech.2016.03.001. Epub 2016 Mar 10.

The influence of the Peroneus Longus muscle on the foot under axial loading: A CT evaluated dynamic cadaveric model study.

Dullaert K1, Hagen J2, Klos K3, Gueorguiev B4, Lenz M5, Richards RG6, Simons P7.

Pincer Toe nails: You've seen them; did you know what they were and how they got that way? Or, did you dismiss them?

Screen Shot 2018-04-06 at 8.13.23 AM.png

We think Hitomi’s hypothesis is correct. Here is why (this is paraphrased from our blog post on subungal hematomas and our revolutionary thinking on why they occur and it seems to fit well with pincer nail formation as well).

… when the skin is pulled at a differential rate over the distal phalange (from gripping of the toes rather than downward pressing through the toe pad) there will be a net lifting response of the nail from its bed as the skin is drawn forward of the backward drawn phalange (there is a NET movement of skin forward thus lifting the nail from its bedding). For an at-home example of this, put your hand AND fingers flat on a table top. Now activate JUST your distal long finger flexors so that only the tip of the fingers are in contact with the table top (there will be a small lifting of the fingers). There should be minimal flexion of the distal fingers at this point. Note the spreading and flattening of the nail. Now, without letting the finger tip-skin contact point move at all from the table, go ahead and increase your long flexor tone/pull fairly aggressively. You are in essence trying to pull the finger backward into flexion while leaving the skin pad in the same place on the table. Feel the pressure building under the distal tip of the finger nail as the skin is RELATIVELY drawn forward.] This is fat pad and skin being drawn forward (relative to the phalange bone being drawn backward) into the apex of the nail. Could this be magnifying the curvature of the nail and not offsetting the “automatic curving and shrinkage” function of the nail ? We think it is quite possible.

We have more to say on this topic, the above is just an excerpt of our blog post. More here, in the link below

Is this a gluteus medius foot targeting problem in swing phase or is this a loss of internal hip rotation? Or . . . .

Is this a gluteus medius foot targeting problem in swing phase or is this a loss of internal hip rotation? Or . . . .

You have to examine your client to know what to treat, a gait analysis or a series of screens is not enough. The saying "an exercise is a test and a test is an exercise" has some sharp edges around it. A screen doesn't tell you what exercise a client necessarily needs or should be prescribed.
This stuff really does matter.
What you see is not the problem , it is their compensatory strategy in coping with a problem. When someone has a pebble in their shoe and they walk on the outside edge of their shoe to avoid the pebble the solution is not to tell them to stop walking on the outside of the shoe, the solution is the de-pebble the shoe. Corrective exercises can be a similar path to this pebble analogy. One must look deeper and beyond what we see in our clients, we merely see how they have adapted, not the problem. A Trendelenburg leaning gait is not met with a solution to prescribe a corrective exercise to correct the lean, the solution is to see why the client is reducing the compressive loading across the hip. Stop giving corrective exercises if you are not examining your client. Yes, that means you need to have hands on diagnostic skills. Sorry.

Loading the wrong pattern drives a compensation, and maybe another problem or a compensation to the compensation deeper.

Loading the pattern that is corrective, the one that solves the deficit leading to the gait you see should be your target. Corrective exercises are supposed to be corrective to the problem, not to the gait aberation you see. Without the exam to solidify proper path, corrective exercises often are directed at the things we see, not the aberation that drove what we see. Be part of your clients solution.
If you aren't examining your client, you don't know for certain what you are actually doing.

This is me, Dr. Allen, i am walking in a matter to prove my point.
Do i have a loss of right internal hip rotation (thus the externally rotated limb?). Do i have a swing leg gluteus medius weakness that is allowing me to adduct the limb rendering a mere foot targeting problem? Do i have weak peronei ? A weak glute max ? A right frontal plane drift that i am avoiding by turning my leg out so i can use my quads to help the deficient glutes better block the frontal plane drift ? I could go on an on as to possible causes.
Or do i merely have a pebble in my shoe?
Mic drop.

To give a corrective exercise you have to know what is wrong. That means you have to have the knowledge and the hands on skills to diagnose the "why". So you can prescribe the correct "how".

Shawn Allen, one of the gait guys

Not moving.

Not moving: the fundamental but neglected motor function.

Have you ever had a client tell you that prolonged standing is their biggest challenge ? "My feet kill me when I have to just stand in a booth at a trade show !" , or "My low back kills me when I stand for 2 hours at a cocktail party". In many of these cases, if they start to move, they feel better. I have plenty of trade show folks complaint of foot pain from the sustained standing. The muscles are under a constant sustained load, there is little to no joint movement, the ligamentous support systems undergo creep, and other things. So, i have them walk back and forth the 5-6 steps within the confines of their trade show booth. Movement is medicine. Sustaining a postural position and thus a fixed joint position over time, even with modest load, is fatiguing and eventually leads to multi-tissue failure. Sustained loading, even when suboptimal, is a problem. The nervous system becomes cranky too as discussed in the abstract below.

Here is an interesting article we are trying to get our hands on (please share if you have access to it). It is not a strong correlation to the discussion above, but there is some conceptual spill over we hope to dive deeper into, perhaps on an upcoming podcast.

Abstract

"The function of the motor system in preventing rather than initiating movement is often overlooked. Not only are its highest levels predominantly, and tonicaly, inhibitory, but in general behavior it is often intermittent, characterized by relatively short periods of activity separated by longer periods of stillness: for most of the time we are not moving, but stationary. Furthermore, these periods of immobility are not a matter of inhibition and relaxation, but require us to expend almost as much energy as when we move, and they make just as many demands on the central nervous system in controlling their performance. The mechanisms that stop movement and maintain immobility have been a greatly neglected area of the study of the brain. This paper introduces the topics to be examined in this special issue of Philosophical Transactions, discussing the various types of stopping and stillness, the problems that they impose on the motor system, the kinds of neural mechanism that underlie them and how they can go wrong.This article is part of the themed issue 'Movement suppression:brain mechanisms for stopping and stillness'."

Philos Trans R Soc Lond B Biol Sci. 2017 Apr 19;372(1718). pii: 20160190. doi: 10.1098/rstb.2016.0190.

Not moving: the fundamental but neglected motor function.
Noorani I1, Carpenter RH2.

Podcast 122: Achilles problems, glutes, & feet.

Key tag words:
neuroscience, elon musk, achilles, tendonitis, tendonopathy, eccentric loading, tendon loading, gluteus maximus, gmax, glutes, abductor hallucis, foot pain, hip biomechanics, navicular drop, BEAR, ACL tear, ACL reconstruction, plantar fascitis
 

Show links:

http://traffic.libsyn.com/thegaitguys/pod_122f.mp3

http://thegaitguys.libsyn.com/podcast-122-achilles-problems-glutes-the-feet
Show sponsors:
 www.newbalancechicago.com


www.thegaitguys.com
That is our website, and it is all you need to remember. Everything you want, need and wish for is right there on the site.
Interested in our stuff ? Want to buy some of our lectures or our National Shoe Fit program? Click here (thegaitguys.com or thegaitguys.tumblr.com) and you will come to our websites. In the tabs, you will find tabs for STORE, SEMINARS, BOOK etc. We also lecture every 3rd Wednesday of the month on onlineCE.com. We have an extensive catalogued library of our courses there, you can take them any time for a nominal fee (~$20).
 
Our podcast is on iTunes, Soundcloud, and just about every other podcast harbor site, just google "the gait guys podcast", you will find us.
 
Show Notes:

Stanford Develops Computer That Literally Plugs Into People's Brains

https://www.entrepreneur.com/article/289645


Elon Musk says humans must become cyborgs to stay relevant. 

https://www.theguardian.com/technology/2017/feb/15/elon-musk-cyborgs-robots-artificial-intelligence-is-he-right

1. achilles tendonopathy:

http://www.jospt.org/doi/abs/10.2519/jospt.2016.6462?platform=hootsuite&code=jospt-site

2. achilles tendinitis and tendonosis.

Ohberg L, Lorentzon R, Alfredson H, Maffulli N. Eccentric training in patients with chronic Achilles tendinosis: normalised tendon structure and decreased thickness at follow up. British Journal of Sports Medicine. 2004;38(1):8-11. doi:10.1136/bjsm.2001.000284.

link to abstract: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1724744/

3. Is Achilles tendon blood flow related to foot pronation?
 E. Wezenbeek,T. M. Willems,N. Mahieu,I. Van Caekenberghe,E. Witvrouw,D. De Clercq

http://onlinelibrary.wiley.com/doi/10.1111/sms.12834/full

4.  The effects of gluteus maximus and abductor hallucis strengthening exercises for four weeks on navicular drop and lower extremity muscle activity during gait with flatfoot

Young-Mi Goo, MS, PT,1 Tae-Ho Kim, PhD, PT,1,* and Jin-Yong Lim, MS, PT1  J Phys Ther Sci. 2016 Mar; 28(3): 911–915.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842464/

5. BEAR
https://www.youtube.com/watch?v=k3g-CagCrZM

Bridge-Enhanced Anterior Cruciate Ligament Repair (BEAR) procedure uses stitches and a bridging scaffold (a sponge injected with the patient’s blood) to stimulate healing of the torn ACL eliminating the need tendon graft.

References:
Murray, M., Flutie, B., Kalish, L., Ecklund, K., Fleming, B., Proffen, B. and Micheli, L. (2016). The Bridge-Enhanced Anterior Cruciate Ligament Repair (BEAR) Procedure: An Early Feasibility Cohort Study. Orthopaedic Journal of Sports Medicine, 4(11).

L. Proffen, B., S. Perrone, G., Roberts, G. and M. Murray, M. (2015). Bridge-Enhanced ACL Repair: A Review of the Science and the Pathway Through FDA Investigational Device Approval. Annals of Biomedical Engineering, 43(3), pp.805-818.

The Circle of Durability.


The article below for some reason inspired today's soft rant. I hope you feel this is worth your time. 
Yesterday I talked about arch height and ankle mortise dorsiflexion and how we can obtain more global dorsiflexion range through some pronation, loosely meaning, some arch compression/drop and splaying apart of the tripod legs of the foot. Global arch flexibility is a piece of that puzzle.  This action of arch compression/drop/tripod splay moves the tibia forward in the sagittal plane and this is global dorsiflexion. Let me be clear however, a reduced ankle mortise dorsiflexion range of sagittal motion which is met by more arch height reduction/prontation/tripod splay, is still dorsiflexion however it is less sagittal dorsiflexion and a little more adduction and medial drift. This can bring the knee into the medial plane and it does promote more internal spin of the limb, this can be a problem.  None the less, it is still global dorsiflexion. It is something we see at the bottom of a squat, we see it because to get there most of us do not have all that dorsiflexion at the mortise. It is not abnormal, the question is, "is it safe for you? Can you do it repeatedly, safely?" It is where we go when we need more sagittal motion, but it may not be ideal, and is often what creates functional pathology. We see it all the time, someone says in an email, "I have plenty of ankle dorsiflexion, that is not my issue".  Do you have plenty? Is it not really your problem? This is fine tuning stuff, it takes a skillful eye and assessment hand. It takes experience to see the whole picture. You cannot get this full 4k experience and understanding from a 2 dimensional youtube video. This arch compression and pronation is normal to occur, it should occur, it must occur. But, how much is too much, for you ? I like to explain it this way, 


"there is a point at which sound, economical, durable, biomechanics becomes a liability. And, at that point where the liabilities begin is in fact where we begin to skirt the edges of that durable skilled movement. Where we begin juggling our liabilities is where the risks begin to mount and begin to whittle away or trump our S.E.S.P (skill, endurance, strength, power). This is where injury often occurs, at that intersection where the gas tank of our S.E.S.P. begins to run low and our liabilities begin to run high." 


Sidebar: 
I have explained this concept many times before when talking about the cross over gait. Moving towards a narrower step width is fine if you have the durability to be there. The question is, how long are you going to be there ? A cross over gait tendency is more economical but you begin to risk liabilities toward injury if that durability becomes challenged. As a runner you must know where your safe zone exists and know how much durability you have at those fringes of your movement. It is when you are there too long, too often, or too much that you empty that durability gas tank which then increases your liabilities towards injury. This is why I give high volume and strength work once a problem is solved, to make sure that they can keep that circle of durability high. It is when we stop keeping our gas tanks large and full that we run on fumes and our risks increase. You might be able to run economically for 5 miles with a narrow step width cross over style running gait. But, can you do it safely at 10 miles ? How about 15?  Is it any wonder why people get injured as they fatigue their safe motor patterns ?  If they have worked hard to keep that circle of durability large (S.E.S.P.) they are bound to be safer and less injured. Injuries occur because we exit our circle of durability, its gas tank has run too low, liabilities now trump economy and durability.

- Dr. Shawn Allen, the gait guys

http://www.japmaonline.org/doi/abs/10.7547/8750-7315-2016.1.Song
 

Toe grip strength and hallux valgus

#craigpayne over at Podiatry Arena said, "chicken or the egg", which came first ?
Weak Toe Grip Strength (TGS) correlates with hallux valgus . . . 
Do not yet take this study as "do more toe grip strength work", that is NOT what it is saying !!!!!!

We have taken note in our clinics that it "appears" that more long hallux flexor use often "seems" to accentuate a hallux valgus (HV). We continue to study this observation, but not hanging our hat on any conclusions as of yet. But, when someone with HV grips with the long toe flexor hammering down the distal toe, the valgus appears to accentuate. We shall see, its an observation. None the less, we try to get these folks into a pressing, then add the long flexor, and this seems to give adequate purchase on the ground without as much valgus posturing. Keep looking into more active toe extension, separation and hallux abduction as a means to an end. This will likely be a discussion on podcast 113, coming soon. Have you listened to podcasts 108 or 109 yet ? 109 launched Saturday. Keep up !

Weak TGS Correlates with Hallux Valgus in 10 12 Year Old Girls: A Cross- Sectional Study

https://www.researchgate.net/publication/304271421_Weak_TGS_Correlates_with_Hallux_Valgus_in_10_12_Year_Old_Girls_A_Cross-_Sectional_Study

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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.

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The partial truth about the Foot Tripod. The HEXApod.

The gait guys have talked about the foot tripod for a very long time. But the truth of the matter is that it is really a HEXApod. HEXA means 6. And when the foot is properly orientated and engaged on the ground, the 5 metatarsal heads and the heel should all be engaged with the ground, truly making it an asymmetrical hexapod. In an ideal scenario, the foot would be most stable if it looked like the strange symmetrical hexapod above with the contact points equally distributed around a center point. But that is not the human foot and this version of a hexapod is far simpler and likely inferior to the foot hexapod when human locomotion is to be attempted. The human foot is engineering marvel when it works properly.  

Perhaps the best example of what I mean by the foot being a HEXApod is in the pressure diagram above. In that first picture, on the right of that picture, we see multiple pressure points under the metatarsal heads of the right foot.  Minus the missing 1st metatarsal head pressure point (taken over by increased flexor hallucis longus activity represented by increased pressure at the big toe),  this pretty much confirms that the foot is not a tripod, rather a hexapod. The theory of the tripod, the 1st and 5th metatarsal heads and the heel, is only crudely accurate and honest. In this picture case, this person has increased lateral foot weight bearing (possibly why the 1st MET head pressure is absent) and possibly represented by pressure under the base of the 5 metatarsal. This is not normal for most people and if this person could get the 1st MET head down, they might even have a HEPTApod foot structure because of the 5th metatarsal base presentation (which sometimes represents peroneal muscle weakness). 

Where did we lead you astray after all these years of “tripod” talk ? We have always discussed the foot tripod. We have always discussed the imperative need to keep the limb’s plumb line forces within the area represented by the tripod.  If your forces fall more laterally within the tripod, as in this first discussed picture, one is at increased risk of inversion events and the myriad of compensations within the entire body that will occur to prevent that inversion. So again, why the tripod?  Well, it is easier to understand and it serves our clients well when it comes to finding active foot arch restoration as seen in this video of ours here.  But, the truth of the matter is that all of the metatarsal heads should be on the ground. The 2nd METatarsal is longer, the 3rd a little shorter, and the 4th and 5th even a little short than those. With the 1st MET shorter, these 5 form a kind of parabolic arc if you will. Each metatarsal head still should contact the ground and then each of those metatarsals should be further supported/anchored by their digits (toes) distally.  So the foot is actually more truly a HEXAPOD. Take the old TRIPOD theory we have always spoken about and extend a curved line beyond the forefoot bipod points (1st and 5th metatarsals) to incorporate contact points on the 2, 3 and 4th metatarsal heads. These metatarsals help to form the TRANSVERSE arch of the foot. It is this transverse arch that has given us the easily explainable foot TRIPOD because if a line is drawn between just the shorter 1st and 5th metatarsals, we do not see contact of the 2-4 metatarsal heads when we only look for pressure between these two bipod landmarks, but the obvious truth is that the 2-4 metatarsals are just longer and extend to the ground further out beyond this theoretical line drawn between the 1st and 5th MET heads.   

So, the foot is a HEXAPOD. Make no mistake about it. It is more stable than a tripod because there are more contact points inside the traditionally discussed foot tripod model. And frankly, the tripod theory is just a lie and just too fundamentally simple, unless you are an American 3 toed woodpecker.

Dr. Shawn Allen,     www.doctorallen.co

one of the gait guys

To met pad or not to met pad; that is the question. 

We use these in practice all the time. Think of it as a “helper” while you are training your patient or client to have better foot mechanics. 

“It’s all about the stress transfer, so what you’re trying to do is unload a certain spot on the foot—generally the met head with a met pad—and transfer it to a more proximal region,” 

Here is a nice evidence based review:

http://lermagazine.com/cover_story/evidence-based-use-of-metatarsal-pads
Social media reader comments and questions:
Reader: You demonstrated a peroneal exercise a few days back. In addition to the use of MT pads, is it effective in supporting transverse metatarsal arch?
  • The Gait Guys It can be. In our opinion, the exercises are key and the pad supports the exercises
  • The Gait Guys the goal is to restore foot function so that you do not need the pad. If your client is patient and willing to work on the exercises you likely won’t need a met pad, they may help speed things up, but remember, it is a crutch and crutches can be helpful but one can get lazy in using them and not do the supportive work. We only try to use them sparingly and only when necessary.
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The case of the dropped (plantarflexed) metatarsal head. Or, “How metatarsalgia can happen”.

This gentleman came in with fore foot pain (3rd metatarsal head specifically), worse in the AM upon awakening, with first weight bearing that would improve somewhat during the day, but would again get worse at the end of the day and with increased activity. The began insidiously a few months ago (like so many problems do) and is getting progressively worse.

Rest and ice offer mild respite, as does ibuprofen. You can see his foot above. please note the “dropped” 3rd metatarsal head (or as we prefer to more accurately say, “plantarflexed 3rd metatarsal head”) and puffiness and prominence in that area on the plantar surface of the foot. 

To fully appreciate what is going on, we need to look at the anatomy of the short flexors of the foot. 

The flexor digitorum brevis (FDB) is innervated by the medial plantar nerve and arises from the medial aspect of the calcaneal tuberosity, the plantar aponeurosis (ie: plantar fascia) and the areas bewteen the plantar muscles. It travels distally, splitting at the metatarsal phalangeal articulation (this allows the long flexors to travel forward and insert on the distal phalanges); the ends come together to divide yet another time (see detail in picture above, yes, we are aware it is the hand, but the tendon structure in the foot is remarkably similar)) and each of the 2 portions of that tendon insert onto the middle of the middle phalanyx (1) 

As a result, in conjunction with the lumbricals, the FDB is a flexor of the metatarsal phalangeal joint, and proximal interphalangeal joint (although this second action is difficult to isolate. try it and you will see what we mean). In addition, it moves the axis of rotation of the metatasal phalangeal joint dorsally, to counter act the function of the long flexors, which, when tight or overactive, have a tendency to drive this articulation anteriorly (much like the function of the extensor hallucis brevis above in the drawing from Dr Michauds book, yes, we are aware this is a picture of the 1st MTP).

Can you see the subtle extension of the metatarsal phalangeal joint and flexion of the proximal interphalangeal joint in the picture?

We know that the FDB contracts faster than the other intrinsic muscles (2), playing a tole in postural stability (3) and that the flexors temporally should contract earlier than the extensors (4), assumedly to move this joint axis posteriorly and allow proper joint centration. When this DOES NOT occur, especially if there is a concomitant loss of ankle rocker, the metatarsal heads are driven into the ground (plantarflexion), causing irritation and pain. Metatarsalgia is born….

So what is the fix? Getting the FDB back on line for one. 

  • How about the toe waving exercise? 
  • How about the lift spread reach exercise? 
  • How about retraining ankle rocker and improving hip extension?
  • How about an orthotic with a metatarsal pad in the short term? 
  • How about some inflammation reducing modalities, like ice and pulsed ultrasound. Maybe some herbal or enzymatic anti inflammatories?

The Gait Guys. Increasing your gait and foot literacy with each and every post. 

1. http://en.wikipedia.org/wiki/Flexor_digitorum_brevis_muscle

2. Tosovic D1, Ghebremedhin E, Glen C, Gorelick M, Mark Brown J.The architecture and contraction time of intrinsic foot muscles.J Electromyogr Kinesiol. 2012 Dec;22(6):930-8. doi: 10.1016/j.jelekin.2012.05.002. Epub 2012 Jun 27.

3.Okai LA1, Kohn AF. Quantifying the Contributions of a Flexor Digitorum Brevis Muscle on Postural Stability.Motor Control. 2014 Jul 15. [Epub ahead of print]

4. Zelik KE1, La Scaleia V, Ivanenko YP, Lacquaniti F.Coordination of intrinsic and extrinsic foot muscles during walking.Eur J Appl Physiol. 2014 Nov 25. [Epub ahead of print]

Podcast 77: Gait analysis, Forefoot Running & more.

Plus, the 5 neurologic gait compensation expressions.

*Show sponsor: www.newbalancechicago.com

A. Link to our server: 

http://traffic.libsyn.com/thegaitguys/pod_77final.mp3

Direct Download: 

http://thegaitguys.libsyn.com/podcast-77

B. iTunes link:

https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138

C. Gait Guys online /download store (National Shoe Fit Certification and more !) :

http://store.payloadz.com/results/results.aspx?m=80204

D. other web based Gait Guys lectures:

www.onlinece.com   type in Dr. Waerlop or Dr. Allen,  ”Biomechanics”

______________

Today’s Show notes:

Google X acquires ‘tremor-canceling spoon’ startup
http://venturebeat.com/2014/09/10/google-x-acquires-tremor-canceling-spoon-startup/

The 5 expressions of neurologic gait decomposition,
Last week we did an online teleseminar … . .
An acoustic startle alters knee joint stiffness and neuromuscular control
http://onlinelibrary.wiley.com/doi/10.1111/sms.12315/abstract
Effectiveness of Off-the-Shelf, Extra-Depth Footwear in Reducing Foot Pain in Older People: A Randomized Controlled Trial
http://biomedgerontology.oxfordjournals.org/content/early/2014/09/08/gerona.glu169.abstract
reader:
I really appreciate learning from you!! I have a bit of a loaded question that I will try to explain clearly to the best of my ability. About 2 years ago, I broke my left shin (hairline-fibula) in a MMA fight. After it healed, a few things have been happening that I assume are connected but can’t quite put my finger on. My ankle mobility on my left ankle is worse than my left. I seem to have permanent turf toe as well. My right glute, ham, and erector are hyperactive.
Additionally, many times when sprinting, pushing a sled, etc, my right quad will become fatigued much more than my left. I believe it’s because I’m not fully extending my left ankle, and relying on my right leg more. Whenever I squat or deadlift, I feel similar too. The right glute and erectors get much more of a “pump” than my left. With all of this, is there anything you would recommend? I truly appreciate it!! It is very frustrating. Thank you again!

Podcast 72: Neuroplasticity, EVA Shoe Foam, and Shoe Trends

Maximalist shoes and the death of Minimalism ? Could this be true ?

*Show sponsor: www.newbalancechicago.com

Lems Shoes.  www.lemsshoes.comMention GAIT15 at check out for a 15% discount through August 31st, 2014.

A. Link to our server: 

http://traffic.libsyn.com/thegaitguys/pod_73f.mp3

Direct Download: 

http://thegaitguys.libsyn.com/podcast-72

B. iTunes link:

https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138

C. Gait Guys online /download store (National Shoe Fit Certification and more !) :

http://store.payloadz.com/results/results.aspx?m=80204

D. other web based Gait Guys lectures:

www.onlinece.com   type in Dr. Waerlop or Dr. Allen,  ”Biomechanics”

______________

Today’s Show notes:

1. Neuroplasticity: Your Brain’s Amazing Ability to Form New Habits
new link (does not have the old photo ivo mentioned that he loved)
 
2. Last week we pounded the sand on EVA foam and maximalist shoes. There was alot of attention, emails and good social media discussion on the topic.  
LETS REVIEW IT
file:///Users/admin/Downloads/p142_Heel_shoe_interactions_and_EVA_foam_f_web_150dpi.pdf
 
3. Then there just last week there was an article in LER on “the death of minimalist shoes” ? 
READ THIS: 
The rise and fall of minimalist footwear | Lower Extremity Review Magazine
http://lermagazine.com/cover_story/the-rise-and-fall-of-minimalist-footwear
 

4.  Physical Therapy as Effective as Surgery for Meniscal Tear

Kathleen Louden

March 20, 2013
Torn Meniscus? Thinking about surgery? Think again…

5. Cast study: the broken foot tripod
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tumblr_n6o2eycOuV1qhko2so2_1280.jpg
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Spanking the orthotic: The effects of hallux limitus on the foot’s longitudinal arch.

But the issues do not stop at the arch. If you have been with us long enough, you will have read about the effects of the anterior compartment (namely the tibialis anterior, extensor digitorum and hallucis and peroneus tertius muscles) strength and endurance on the arch.

Here we have a very troubled foot. This foot has undergone numerous procedures, sadly. Today we will not talk about the hallux varus you see here, a virtual unicorn in practice  (and acquired in this case) nor do we want to discuss the phalangeal varus drift. We want to draw your attention to the obvious impairment of the 1st MTP (metatarsophalangeal joint) dorsiflexion range.  You can see the large dorsal crown of osteophytes, a dorsal buttress to any hallux dorsiflexion.  There is under 10 degrees of dorsiflexion here, not even enough worth mentioning.  We have said it many times before, if you lose a range at one joint usually that range has to be accommodated for proximal or distal to the impaired joint. This is a compensation pattern and you can see it here in the hallux joints themselves.

Here you can see that some of the dorsiflexion range has been acquired in the proximal phalangeal joint.  We like to call this “banana toe” when explaining it to patients, it is a highly technical term but you are welcome to borrow it. This occurred because the joint was constantly seeing the limitation of dorsiflexion of the 1st MTP joint and seeing, and accommodating to, the demands of the need for more dorsiflexion at toe off. 

But, here is the kicker. You have likely seen this video of ours on Youtube on how to acquire a foot tripod from using the toe extensors to raise the arch.  Video link here  and here.  Well, in his patient’s case today, they have a limitation of 1st MTP dorsiflexion, so the ability to maximally raise the arch is impaired. The Windlass mechanism is broken; “winding” of the plantar fascia around the !st MTP mechanism is not sufficiently present. Any limitations in toe extension (ie dorsiflexion) or ankle dorsiflexion will mean that :

1. compensations will need to occur

2. The Windlass mechanism is insufficient

3. gait is impaired at distal swing phase and toe off phases

4. the anterior compartment competence will drop (Skill, endurance, strength) and thus injury can be more easily brought to the table.

In this patient’s case, they came in complaining of burning at the top of the foot and stiffness in the anterior ankle mortise area.  This would only come on after a long brisk walk.  If the walk was brisk yet short, no problems. If the walk was long and slow, no problems.  They clearly had an endurance problem and an endurance challenge in the office showed an immediate failure in under 30 seconds (we will try to shoot a quick video so show our little assessment so be patient with us). The point here today is that if there is a joint limitation, there will be a limitation in skill, strength or endurance and very likely a combination of the 3. If you cannot get to a range, then any skill, endurance or strength beyond that limitation will be lost and require a compensation pattern to occur.  This patient’s arch cannot be restored via the methods we describe here on our blog and it cannot be restored by an orthotic. The orthotic will likely further change, likely in a negative manner, the already limited function of the 1st MPJ. In other words, if you raise the arch, you will shorten the plantar fascia and draw the 1st MET  head towards the heel (part of the function of the Windlass mechanism) and by doing this you will plantarflex the big toe … .  but weren’t we praying for an increase in dorsiflexion of the limitus big toe ? ……..yes, exactly !  So use your head  (and spank the orthotic when you see it used in this manner.  ”Bad orthotic, bad orthotic !”)

So think of all of this the next time you see a turf toe / hallux rigidus/ hallux limitus. Rattles your brain huh !?

This is not stuff for the feint of heart. You gotta know your biomechanics.

Shawn and Ivo … .the gait guys

Addendum for clarity:

a Facebook reader asked a question:

From your post: “if you raise the arch, you will shorten the plantar fascia and draw the 1st MET head towards the heel (part of the function of the Windlass mechanism) and by doing this you will plantarflex the big toe … . but weren’t we praying for an increase in dorsiflexion of the limitus big toe ? ” I always thought when the plantar fascia is shortened, it plantar flexes the 1st metatarsal (1st ray) and extends (dorsiflexes) the 1st MTP joint….

Our response:  

We should have been more clear, our apologies dear reader.  Here is what we should have said , ” The plantar fascia is non-contractile, so it does not shorten. We meant conceptually shorten. When in late stance phase, particularly at toe off when the heel has raised and forefoot loading is occurring, the Windlass mechanism around the 1st MET head (as the hallux is dorsiflexing) is drawing the foot into supination and thus the heel towards the forefoot (ie passive arch lift). This action is driving the 1st MET into plantarflexion in the NORMAL foot.  This will NORMALLy help with increasing hallux dorsiflexion. In this case above, there is a rigid 1st MTP  joint.  So this mechanism cannot occur at all. In this case the plantar fascia will over time retract to the only length it does experience. So, if an orthotic is used, it will press up into the fascia and also plantarflex the 1st MET, which will carry the rigid toe into plantar flexion with it, IN THIS CASE.”

A case of plantar foot pain during gait.  
 This client came to see us after a surgical proceedure to remove a dead (osteonecrosis) medial sesamoid under the 1st metatarsal head and a later surgery to fix a progressing hammer toe of the 2nd digit. What we really want you to see is the huge divot/depression under the 2-3 metatarsal heads. Also note the accumulation and relocation of the normal MET head fat pad now located distal to the MET heads.  It is as if the fat pad is trying to hitch a ride on the toes now ! This is a case of Metatarsalgia secondary to fat pad displacement (displaced from the divot area to the flexor crease) secondary to surgical sequelae.  
 What is additionally cool in this case is the fact that this client has an almost complete webbing of the 2-3 toes so many of the normal independent muscular functions are no longer independent. After the surgeries this person presents with tremendous loss of flexor and extensor function of the 2-3 toes.  Lumbrical testing was most obviously impaired, completely absent in fact, in these 2-3 toes. On the ground the patient was also unable to achieve any flexion-press of the toes into the ground, he was able to flexion/hammer curl which will obviously put them at risk for hammer toes in the future.  But what is important here is that without the ability to PRESS the toes into the ground particularly while in stance phase the lumbricals will not help to hold the fat pad in its normal location under the MET heads. Nor will they be able to to perform their other major functions, namely:  thinking from a distal to proximal orientation (a closed chain  mode of thinking), they actually plantarflex the metatarsal on the fixed  phalynx, assist in dorsiflexion of the ankle, and help to keep the toes  from clawing from over recruitment of the flexor digitorum longus.   
 This client’s MET head pain is obviously caused by lack of cushioning of the head since the fat pad is displaced. There are plenty of other biomechanical abberancies now, the Windlass mechanism will never be the same becuase it is without one of the sesamoids, the hallux short flexor (FHB) is impaired on the medial head without the sesamoid so hallux flexion will become a problem.  Do we really want to see such compromise of the medial tripod ? Heck no, we need sesamoid implants ! There is a novel idea ! When a sesamoid is taken out we need to replace it ! Think about it ! 
 There is so much more to this case, but we will stop here. It’s Christmas after all ! This poor lady was told to wish from Santa for a medial sesamoid implant under the tree and a sudden spontaneous activation of the lumbricals to retract the fat pad back under the MET head so as to reduce her pain.  Hey, wishing can’t hurt ! 
   Merry Christmas and Happy Holidays to you all gang, whatever your faith we wish you well,   
    from Shawn and Ivo…… The Gait Guys   
 (PS: we included below more from the body of the article we wrote long ago called “The Lost Lumbricals”.  So for those of you who wish to geek out more on Christmas, read on … 
 ______________ 
   EXCERPTS FROM “THE LOST LUMBRICALS”   
 The lumbricals of the foot attach proximally to the sides of adjacent  tendons of the flexor digitorum longus (with the exception of the 1st, which only attaches to the medial side) and attach distally to the medial aspect of the head of the proximal phalynx and continue on to the extensor hoods in toes 2 through 5. Their typical function is described as flexion of the proximal phalynx and extension of the proximal and distal interphalangeal joints. They have the unique ability to compress the metatarsal-phalangeal and interphalangeal joints. These are “open chain” functions as described, unless you are in the habit of waving to people with your toes, they often are used quite differently in the gait cycle with the foot affixed to the ground.  The lumbricals are most active from midstance to preswing. That means they act predominantly in the closed chain. The lumbricals, along with the other intrinsic muscles of the foot, play a role in maintaining the medial longitudinal arch of the foot.  Along with the interossei, they play a role in stabilization of the forefoot during stance phase and rearfoot during preswing. One author has proposed that overpronation is due to a lack of neuromuscular control of the intrinsic foot muscles to stabilize the tarsal and metatarsal bones and therefore modulate the speed of pronation.    Thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.    Clawing toes during gait, which are considered abnormal, are defined as extension of the metatarsophalangeal articulation, and flexion of the proximal and distal interphalangeal joints result from a foot attempting to stabilize itself during the terminal stance and preswing phases of gait.  This is an attempt to help propel the body forward, often accompanied by overactivity of the flexor digitorum longus, tibialis posterior, flexor pollicus longus, and gastroc soleus groups. Overactivity of these groups causes reciprocal inhibition of the long toe extensors and ankle dorsiflexors (tibialis anterior for example), causing the toes to buckle further and a loss of ankle dorsiflexion; in short, diminished ankle rocker.  Now think about the changes in the gait cycle in the above scenario. There will be a resultant shortened step length, diminished ankle rocker, increased forefoot rocker and premature heel rise. This will necessitate an increased extension at the metatarsophalangeal joints, shifting the tendon of the lumbricals upward and behind the transverse metatarsal joint axis, causing even more extension now at this joint.  Chronically over time, this causes displacement of the fat pads anteriorly from under the metatarsal heads and is one of the main reasons metatarsal head pain (metatarsalgia).  In the past have you made the apparent simple diagnoses of metatarsalgia, shin splints, stress fractures or Morton’s neuroma without knowing a more plausible cause ?  Do you now feel you have better answers to these clinical phenomena ?  Now think about changes up the kinetic chain and the potential musculoskeletal implications of muscle inhibition, overfacilitation and joint dysfunction, often with neurological sequelae. With lumbrical dysfunction (weakness) and the resultant lack of ankle dorsiflexion, you have less hip extension.  So, you borrow some from the lumbar spine, with increased compressive forces there and an increase in the lordosis, which causes an increase in the thoracic kyphosis and cervical lordosis. We still need to get this leg up and forward to continue our progression ahead, so now we fire our hip flexors instead of the abdominal obliques. And because there needs to be cooperation of the abdominals and hamstrings to maintain pelvis neutrality, this further fuels inhibition of the gluteals thus further compounding the loss of hip extension. Now how about a little increased shoulder flexion on the contralateral side to assist getting that leg forward? Don’t forget that we have altered the thoracic kyphosis and thus changed scapulo humeral mechanics. Now neck/shoulder pain all from bad feet?  Maybe. These muscles developed and exist for a good reason, do your best not to dismiss them and their function the next time you see a tortured foot.  When patients have continued dysfunction, consider the base and where it all begins. Consider function in the context of where it occurs. Proper evaluation of the feet and gait can provide valuable clues as to the etiology or manifestation of continued problems. Important? You decide.

A case of plantar foot pain during gait.

This client came to see us after a surgical proceedure to remove a dead (osteonecrosis) medial sesamoid under the 1st metatarsal head and a later surgery to fix a progressing hammer toe of the 2nd digit. What we really want you to see is the huge divot/depression under the 2-3 metatarsal heads. Also note the accumulation and relocation of the normal MET head fat pad now located distal to the MET heads.  It is as if the fat pad is trying to hitch a ride on the toes now ! This is a case of Metatarsalgia secondary to fat pad displacement (displaced from the divot area to the flexor crease) secondary to surgical sequelae. 

What is additionally cool in this case is the fact that this client has an almost complete webbing of the 2-3 toes so many of the normal independent muscular functions are no longer independent. After the surgeries this person presents with tremendous loss of flexor and extensor function of the 2-3 toes.  Lumbrical testing was most obviously impaired, completely absent in fact, in these 2-3 toes. On the ground the patient was also unable to achieve any flexion-press of the toes into the ground, he was able to flexion/hammer curl which will obviously put them at risk for hammer toes in the future.  But what is important here is that without the ability to PRESS the toes into the ground particularly while in stance phase the lumbricals will not help to hold the fat pad in its normal location under the MET heads. Nor will they be able to to perform their other major functions, namely: thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

This client’s MET head pain is obviously caused by lack of cushioning of the head since the fat pad is displaced. There are plenty of other biomechanical abberancies now, the Windlass mechanism will never be the same becuase it is without one of the sesamoids, the hallux short flexor (FHB) is impaired on the medial head without the sesamoid so hallux flexion will become a problem.  Do we really want to see such compromise of the medial tripod ? Heck no, we need sesamoid implants ! There is a novel idea ! When a sesamoid is taken out we need to replace it ! Think about it !

There is so much more to this case, but we will stop here. It’s Christmas after all ! This poor lady was told to wish from Santa for a medial sesamoid implant under the tree and a sudden spontaneous activation of the lumbricals to retract the fat pad back under the MET head so as to reduce her pain.  Hey, wishing can’t hurt !

Merry Christmas and Happy Holidays to you all gang, whatever your faith we wish you well,

from Shawn and Ivo…… The Gait Guys

(PS: we included below more from the body of the article we wrote long ago called “The Lost Lumbricals”.  So for those of you who wish to geek out more on Christmas, read on …

______________

EXCERPTS FROM “THE LOST LUMBRICALS”

The lumbricals of the foot attach proximally to the sides of adjacent  tendons of the flexor digitorum longus (with the exception of the 1st, which only attaches to the medial side) and attach distally to the medial aspect of the head of the proximal phalynx and continue on to the extensor hoods in toes 2 through 5. Their typical function is described as flexion of the proximal phalynx and extension of the proximal and distal interphalangeal joints. They have the unique ability to compress the metatarsal-phalangeal and interphalangeal joints. These are “open chain” functions as described, unless you are in the habit of waving to people with your toes, they often are used quite differently in the gait cycle with the foot affixed to the ground.

The lumbricals are most active from midstance to preswing. That means they act predominantly in the closed chain. The lumbricals, along with the other intrinsic muscles of the foot, play a role in maintaining the medial longitudinal arch of the foot.  Along with the interossei, they play a role in stabilization of the forefoot during stance phase and rearfoot during preswing. One author has proposed that overpronation is due to a lack of neuromuscular control of the intrinsic foot muscles to stabilize the tarsal and metatarsal bones and therefore modulate the speed of pronation.

Thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

Clawing toes during gait, which are considered abnormal, are defined as extension of the metatarsophalangeal articulation, and flexion of the proximal and distal interphalangeal joints result from a foot attempting to stabilize itself during the terminal stance and preswing phases of gait.  This is an attempt to help propel the body forward, often accompanied by overactivity of the flexor digitorum longus, tibialis posterior, flexor pollicus longus, and gastroc soleus groups. Overactivity of these groups causes reciprocal inhibition of the long toe extensors and ankle dorsiflexors (tibialis anterior for example), causing the toes to buckle further and a loss of ankle dorsiflexion; in short, diminished ankle rocker.

Now think about the changes in the gait cycle in the above scenario. There will be a resultant shortened step length, diminished ankle rocker, increased forefoot rocker and premature heel rise. This will necessitate an increased extension at the metatarsophalangeal joints, shifting the tendon of the lumbricals upward and behind the transverse metatarsal joint axis, causing even more extension now at this joint. Chronically over time, this causes displacement of the fat pads anteriorly from under the metatarsal heads and is one of the main reasons metatarsal head pain (metatarsalgia). In the past have you made the apparent simple diagnoses of metatarsalgia, shin splints, stress fractures or Morton’s neuroma without knowing a more plausible cause ?  Do you now feel you have better answers to these clinical phenomena ?

Now think about changes up the kinetic chain and the potential musculoskeletal implications of muscle inhibition, overfacilitation and joint dysfunction, often with neurological sequelae. With lumbrical dysfunction (weakness) and the resultant lack of ankle dorsiflexion, you have less hip extension.  So, you borrow some from the lumbar spine, with increased compressive forces there and an increase in the lordosis, which causes an increase in the thoracic kyphosis and cervical lordosis. We still need to get this leg up and forward to continue our progression ahead, so now we fire our hip flexors instead of the abdominal obliques. And because there needs to be cooperation of the abdominals and hamstrings to maintain pelvis neutrality, this further fuels inhibition of the gluteals thus further compounding the loss of hip extension. Now how about a little increased shoulder flexion on the contralateral side to assist getting that leg forward? Don’t forget that we have altered the thoracic kyphosis and thus changed scapulo humeral mechanics. Now neck/shoulder pain all from bad feet?  Maybe. These muscles developed and exist for a good reason, do your best not to dismiss them and their function the next time you see a tortured foot.

When patients have continued dysfunction, consider the base and where it all begins. Consider function in the context of where it occurs. Proper evaluation of the feet and gait can provide valuable clues as to the etiology or manifestation of continued problems. Important? You decide.

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The Quadratus plantae (Flexor accessorius) muscle. Do you have foot pain ?

(*There are two pictures here on the blog. Move your cursor over to the side of the photo and you will see that you can toggle between the photo and anatomy pic).

This is a great, but highly overlooked, muscle.  The QP acts to assist in flexing the 2nd to 5th toes.  Equally important is its effect of offsetting the oblique pull of the long toe flexor group (flexor digitorum longus). It has two heads, medial and lateral.  The medial head is attached to the calcaneus, while the lateral head originates from the lateral border of the calcaneus, in front of the lateral process of the calcaneal tuberosity and the long plantar ligament.

The fact that we just love, and one that we believe is often overlooked is the acute angle at which the muscle heads attach into the tendons of the flexor digitorum longus (see picture) and has a rather dramatic alignment effect on the lateral 3 digits (since the line of pull on the long flexor tendons to these 3 digits is most dramatically changed by the purely posterior pull of the Quadratus Plantae.  As you can see in this stripped down anatomy picture, without the QP pulling on the tendons of the FDL to these 3 lateral toes, those toes will have to curl medially and gently flex (*see the photo, a classic presentation!)  By having a competent and active QP that oblique line of pull of the FDL /long flexors is rearranged to be more of a pure posterior pull and you will not see this classic lateral 3 digit curl and medial drift. This action is accentuated in a cavus foot type, where the pull of the FDL will be accentuated, due to the mechanical advantage afforded it and relative adduction of the forefoot with respect to the rear foot.

In the photo you can see a classic representation of a deficient Quadratus Plantae, in this case the patients lateral head was dramatically weaker than the medial, but both were weak.  So, summary time….if you know your anatomy, know your biomechanics, and if you can test the muscle bundles specifically……..then you can see why form follows function (and in this case, why form has followed dysfunction).  As we always say, “ya gotta know your stuff”, and you have to test what you suspect……there are other things that could also do this……so, let your eyes gain info, let your brain process and prove or disprove the information.

we are…….the gait guys !