The Tib Posterior...Revisited...

Posterior tibialis tendinitis is a primary soft tissue tendinopathy of the posterior tibialis that leads to altered foot biomechanics. Although the natural history of posterior tibialis tendon dysfunction is not fully known, it has mostly been agreed that it is a progressive disorder.(1)

The tibialis posterior originates from the proximal posterior tibia and fibula and interosseous membrane; it is deep in the posterior compartment of the leg and changes its line of pull from the vertical to horizontal at the medial malleolus. The musculotendinous junction is in the distal third of the leg and the tendinous portion turns 90 degrees at the medial malleolus. It has a broad insertion into the plantar surface of the midfoot, largely into the navicular tuberosity with branches to the sustentaculum tali, and the remainder inserting into the entire plantar midfoot except for the 5th metatarsal(1-3).

 The tibialis posterior (TP) is one of the more important extrinsic arch stabilizing muscles. It is a stance phase muscle that fires from the loading response through terminal stance, acts eccentrically to loading response to mid stance to slow pronation and concentrically from mid stance to terminal stance to assist in supination.(4) Its recruitment seems to be increased with slower walking speeds (5).

Since the foot is usually planted when it fires, we must look at its closed chain function (how it functions when the foot/insertion is fixed on the ground), which is predominantly maintenance of the medial longitudinal arch, with minor contributions to the transverse metatarsal and lateral longitudinal arches (6) ; flexion and adduction of the tarsal’s and metatarsals and eccentric slowing of anterior translation of the tibia during ankle rocker. It is also an external rotator of the lower leg and is the prime muscle which decelerates internal rotation of the tibia and pronation. As the origin and insertion are concentrically brought towards each other during early passive heel lift it becomes a powerful plantarflexor and inverter of the rearfoot.  There is also a  component of ankle stabilization via posterior compression of the tarsal’s and adduction of the tibia and fibula.

Alas, there is much more than the typical open chain functions of plantar flexion, adduction and inversion. Perhaps it is some of these other, closed chain functions, that cause the “progressive nature of posterior tibial tendon dysfunction"(7)?

This muscle is easily accessed through the posterior compartment, lying deep in the midline to the gastroc and soleus (8,9). Care should be taken to avoid the sural nerve, often found between the heads of the gastroc and becoming superficial (and palpable) in the midline where it exits from the inferior junction of the 2 heads of the gastroc (10). The posterior tibial artery, vein and nerve lie on top of the tibialis posterior for the upper 2/3 of its route through the calf, becoming superficial (and palpable) in the distal 1/3 of the lower leg (11). I find starting laterally or medially and angling your fingers, instrument or the needle medially or laterally seems to work best. Make sure to count your layers!

1. Ling SK, Lui TH. Posterior Tibial Tendon Dysfunction: An Overview.  Open Orthop J. 2017 Jul 31;11:714-723. doi: 10.2174/1874325001711010714. eCollection 2017. link to free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620404/

2. Blake R.L., Anderson K., Ferguson H. Posterior tibial tendinitis. A literature review with case reports. J. Am. Podiatr. Med. Assoc. 1994;84(3):141–149. doi: 10.7547/87507315-84-3-141. [PubMed] [Cross Ref]

3. Supple K.M., Hanft J.R., Murphy B.J., Janecki C.J., Kogler G.F. Posterior tibial tendon dysfunction. Semin. Arthritis Rheum. 1992;22(2):106–113. doi: 10.1016/0049-0172(92)90004-W. [PubMed] [Cross Ref]

4. Semple R, Murley GS, Woodburn J, Turner DE. Tibialis posterior in health and disease: a review of structure and function with specific reference to electromyographic studies. Journal of Foot and Ankle Research. 2009;2:24. doi:10.1186/1757-1146-2-24.

link to free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739849

5. Murley GS1, Menz HB2, Landorf KB2.  Electromyographic patterns of tibialis posterior and related muscles when walking at different speeds. Gait Posture 2014 Apr;39(4):1080-5. doi: 10.1016/j.gaitpost.2014.01.018. Epub 2014 Feb

6. Kaye RA1, Jahss MH.  Tibialis posterior: a review of anatomy and biomechanics in relation to support of the medial longitudinal arch. Foot Ankle. 1991 Feb;11(4):244-7.

7. Rabbito M, Pohl MB, Humble N, Ferber R. Biomechanical and Clinical Factors Related to Stage I Posterior Tibial Tendon Dysfunction.  J Orthop Sports Phys Ther, Epub 12 July  2011.doi:10.2519/jospt.2011.3545.

 8. Howitt S, Jung S, Hammonds N. Conservative treatment of a tibias posterior strain in a novice triathlete: a case report. J Can Chiropr Assoc. 2009 Mar;53(1):23-31.   link to free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652628/

9.   Lou XF, Yang XD, Jiang SH, Sun CY, Zhang RF.[Study on angle and depth of needle insertion in acupuncture at Zusanli (ST 36)]. Zhongguo Zhen Jiu. 2006 Jul;26(7):483-6

10. https://functionalanatomyblog.com/2009/11/26/the-sural-nerve-anatomy-and-entrapment/

11. Enrique Ginzburg, ... Norman M. Rich VASCULAR ANATOMY OF THE EXTREMITIES in Current Therapy of Trauma and Surgical Critical Care, Mosby; Pages 467–472 2008

A little more on the tibialis posterior (or any tendon for that matter)....

We tend to think of the etiology of tendinopathies as being overuse or biomecanically stressful situations, which are often true, but have you thought about vascularization? My partner Dr Allen wrote a great post on vascularization in a yo yo professional here. It has to make you think...

I wrote about posterior tibial tendinopathies in a post a few days ago. A recent paper shows that vascularization can be a major player in posterior tibial tendinopathies (1). Tendon blood flow tends to decrease with age and compression, which often results from increased mechanical load. This decreased vascularization, at least theoretically, can contribuute to the probability of tissue damage as tissue compliance and flexibilty will be compromised (LER). Oxygen consumption of ligaments and tendons is 7.5% lower than skeletal muscle, which may contribute to longer healing times (2,3).

So, how can we increase vascularization?
 

• Aerobic conditioning increases mitochondrial content, myoglobin content and capillary number, among other things, due to increased demand (4).
• Manipulation, mobilization and massage, locally as well as segmentally, can increase blood flow, at least temporarily (5,6). The L4-S1 segments of the posterior tibial nerve are the segmental levels for the tibialis posterior .
• How about some moist heat to cause local peripheral vasodilation?
• I wrote a commentary on how needling can effect local vasodilation here (7), based on this article (8).
• Tissue engineering with various techniques is an upcoming and promising field (9)
• the early research on laser therapy (photobiomodulation) has shown some positive outcomes (10)

Finally, there is some great information about medications and current research from The Angiogenesis Foundation (11)

Adding a modality like needling or acupuncture, combined with exercise and some moist heat and perhaps some laser may help to improve your outcomes. There appears only upside potential and the methods are easy to apply and implement.

1. Geideman WM, Johnson JE. Posterior tibial tendon dysfunction. J Orthop Sports Phys Ther 2000;30(2):68‐

2. Patla CE, Abbott JH. Tibialis posterior myofascial tightness as a source of heel pain: diagnosis and treatment. J Orthop Sports Phys Ther 2000;30(10):624‐

3. Vailas AC, Tipton CM, Laughlin HL, et al. Physical activity and hypophysectomy on the aerobic capacity of ligaments and tendons. J Appl Physiol 1978;44(4):542-546.

4. https://www.cdc.gov/nccdphp/.../chap3.pdf

5.Pickar JG Neurophysiological effects of spinal manipulation. Spine J. 2002 Sep-Oct;2(5):357-71.

6. http://emedicine.medscape.com/article/324694-overview

7. http://www.rehabchalktalk.com/dry-needling-and-vascular-changes

8. BMC Complement Altern Med. 2015; 15: 72. Published online 2015 Mar 20. doi:  10.1186/s12906-015-0587-6PMCID: PMC4426539 Intensive vasodilatation in the sciatic pain area after dry needling

The Fudge Factor

The Fudge Factor

It is often easier to accomplish a task faster, rather than slower (like an exercise or skiing) because of the cortex “interpolating” or making its “best guess” as to what (based on experience) is going to happen. There is a certain amount of guess work (or what we call “the fudge factor”) involved.

Walking at a slower speed (or performing an exercise at a slower speed for that matter) has increased muscular demands, than doing it more quickly. Here is one study that exemplifies that.

“These findings may reflect a relatively higher than expected demand for peroneus longus and tibialis posterior to assist with medio-lateral foot stability at very slow speeds”

Gait Posture. 2014 Apr;39(4):1080-5. doi: 10.1016/j.gaitpost.2014.01.018. Epub 2014 Feb 6.
Electromyographic patterns of tibialis posterior and related muscles when walking at different speeds.
Murley GS1, Menz HB2, Landorf KB2.

The effect of walking speed on superficial lower limb muscles, such as tibialis anterior and triceps surae, is well established. However, there are no published data available for tibialis posterior - a muscle that plays an important role in controlling foot motion. The purpose of this study was to characterise the electromyographic timing and amplitude of selected lower limb muscles across five walking speeds. Thirty young adults were instructed to walk barefoot while electromyographic activity was recorded from tibialis posterior and peroneus longus via intramuscular electrodes, and medial gastrocnemius and tibialis anterior via surface electrodes. At faster walking speeds, peak electromyographic amplitude increased systematically during the contact and midstance/propulsion phases. Changes in the time of peak amplitude were also observed for tibialis posterior, tibialis anterior and peroneus longus activity; however, these were muscle and phase specific. During contact phase, peak electromyographic amplitude for tibialis posterior and peroneus longus was similar across very slow to slow walking speeds. During midstance/propulsion phase, peak electromyographic amplitude for tibialis posterior and medial gastrocnemius was similar across very slow to slow walking speeds. These findings may reflect a relatively higher than expected demand for peroneus longus and tibialis posterior to assist with medio-lateral foot stability at very slow speeds. Similarly, peak amplitude of medial gastrocnemius was also relatively unchanged at the very slow speed, presumably to compensate for the reduced forward momentum. The data presented in this study may serve as a reference for comparing similarly matched participants with foot deformity and/or pathological gait.

Copyright © 2014 Elsevier B.V. All rights reserved.

‪#‎gait‬
‪#‎thegaitguys‬

Here is a great case from a reader.

“Hey guys, I absolutely love the show, especially as it becomes less and less over my head.

Due to your love of gait-altering absurdly thick EVA midsoles, I thought you might like to check out this Hoka incident that occurred at the Marathon des Sable across the Sahara in Morocco, a 6 day 251km event. It was posted by Ian Corless at Talk Ultra Podcast. Apparently the medial side of the midsole collapsed–on DAY 2! This guy finished the race, and as you have to carry 100% of your gear and nutrition, I guess he only had the one pair. It looks like this runner should fly out to CO or IL asap, because if he didn’t have gait issues before, he is sure to have them now.”

This brings up some scary thoughts when it comes to the amount of EVA foam and quality of foam (EVA or otherwise) being used in some shoes.  "The more foam there exists, the greater one can break down into their compensation or deforming strategy.“ What do we mean by this ?  Well, two things should be on one’s mind:  1. all foam breaks down into the vector of the deforming forces and 2. most of us do not have perfectly clean biomechanics, thus an abnormal loading vector is most likely present. These aberrant biomechanics are eventually reflected into our shoes as a "wear pattern”.  In this case, the EVA foam had progressively broken down into their rearfoot pronation (and likely mid and forefoot pronation). In this case, even if the person had enough tibialis posterior and other medial pronation-decelerating structure strength at the start, the acceleration of their foot into this issue is now even more abrupt, brisk, excessive etc.  A new pair of shoes would not be broken down into this deformity and so a newer pair of shoes is preventive. This is why we recommend new shoes often, and the cycling in of another pair (or several pair) into the mix so that one is never driving the same shoes into the potentially destructive compensation patterns that most of us  have.  At least with a fresh pair of shoes brought into the mix at the 200 mile wear point, you would only be in the more destructive shoes every other run, giving the body time to recuperate more. 

As for this pair of shoes, this runner either has a terrible right foot problem or this was a brutally flawed right shoe from the get go, or both. We can only imaging how painful the medial knee might be at this point.  Furthermore, imagine the abrupt nature of the hip internal rotation mechanics ! IF they do not have hip labrum impingement yet, they will soon !  And with that amount of internal limb spin, can you imagine how inhibited the glutes would be from constantly having to eccentrically control that excessive rotation? 

As a whole, are not huge fans of the HOKA shoe family, we just cannot fathom the need for this much foam under the feet. If you have been with us long enough you will have heard on our podcast and blog talk about increased impact forces with increasing EVA foam thickness (want that info, here is the link and references). Just because some EVA foam is good, doesn’t mean more is better.  Remember, to propulse off of a foam infrastructure you must bottom out/compress the foam sufficiently to find a firmness to propulse from. The Hoka’s have plenty of foam making this our concern, and we are not picking on just them. There are other companies doing this “super sizing/super stacking” such as Brooks, Altra, and New Balance to name just a few.  Sure they have added a greater forefoot rocker/toe spring on the front of the shoe to help (they have to because the foam thickness is so great that there is no flexing of the forefoot of the shoes), but is it enough for you? Remember, every biomechanical phase of the gait cycle is necessary and timely to engage the natural joint, ligament, muscle components of joint loading, mobility, stability and movement. If you spend too much time in one phase (perhaps because you are waiting for foam to decompress) you may wait a moment too long and miss the opportunity for another critical phase to begin in the sequence.  This is the root cause of many injuries, aberrant biomechanics leading to aberrant mobility or stability. 

So remember these few things:

1. more is not always better for you, it may be for some, but maybe not you.

2. there is a price to pay somewhere in the mechanical system, after all the body is a contained system. What doesn’t happen at one joint often has to be made up at the next proximal or distal joint.

3. Everyone has some aberrant mechanics. No one is perfect. These imperfections will reflect in your shoes, and the longer you are in a pair of shoes the deeper the aberrant mechanics will be reflected in your shoe, thus acting as a steering wheel for the aberrant pattern (the steering is more direct/ more aggressive than in a new pair of shoes). So keep at least 2 pair of shoes rotating in your run cycle, one newer and one half done. We even recommend 3 pairs often.  Trust us, the sudden biomechanical shift from a dead shoe into a new one (even though it is a clean new shoe without bad patterns in it) is still a biomechanical shift and could cause adaptive phase problems, pain or injury.

Lots to consider in this game. It is not just about dropping into barefoot and taking off down your street. Not if you want to be doing this for a long time and stay healthy.

Shawn and Ivo, the gait guys

* next day follow up from our social media pages:

Along the lines of EVA and yesterdays post: 

“Wear of the EVA consistently increased heel pad stresses, and reduced EVA thickness was the most influential factor, e.g., for a 50% reduction in thickness, peak heel pad stress increased by 19%. ”

This study looks at a model; it would be interesting to see this study with a large cohort.

Biomed Mater Eng. 2006;16(5):289-99.

Role of EVA viscoelastic properties in the protective performance of a sport shoe: computational studies.

Even-Tzur N1, Weisz E, Hirsch-Falk Y, Gefen A.

http://www.ncbi.nlm.nih.gov/pubmed/17075164

Tibialis posterior

A question from one of our readers:

Hi guys,

What are your favourite tib post strengthening exercises or do you usually stay with the anterior strength work?

Thanks

D

Our Response:

Hi,
Thanks for your question. As you know the tibialis posterior muscle from the interosseous membrane, lateral part of the posterior surface of the tibia, and superior two-thirds of the medial surface of the fibula. It travels between the flexor digitorum longus and flexor hallucis longus to insert into the tuberosity of the navicular, cuneiforms, cuboid, and the bases of the 2-4th metatarsals.

The function of the tibialis posterior is one of ankle plantar flexion, calcaneal inversion and plantar flexion as well as stabilization (through compression) of the first ray complex (talus, medial cuneiform, navicular and base of the first metatarsal). It acts additionally to help decelerate subtalar pronation. Further stabilization of the midfoot comes from smaller tendon slips inserting onto the other cuneiforms, metatarsals, the cuboid and the peroneus longus tendon.

The more common problems that can occur with the tibialis posterior complex are those of muscular strain, tendonitis, tendon insufficiency (stretch) and partial or complete tears. Excessive or prolonged pronation causes excessive dorsiflexion of the distal first ray complex, increased pronatory effects, and as discussed above, dysfunction of the 1st MPJ joint. The dorsiflexed 1st toe will compromised the efficiency of the windlass mechanism which “winds up” the plantar fascia, properly positions the paired sesamoids, and thus limit effective dorsiflexion of the 1st MPJ. This dorsiflexion of the first ray requires the tibialis posterior to undergo excessive eccentric load for a longer period of time, thus placing more stress on the tendon and muscle belly.

Clinically we find that more people are flexor driven. Therefore we work quite a bit with increasing extensor function, thus a lot of our rehab protocals involve strengthing Anterior Tib as opposed to Posterior Tib. To this one must ask what is your criterior for strengthening the posterior tib, if over pronation or navicular drop has led you to this conclusion then you may want to reexamine the clinical findings for what muscles may actually be involved.

That being said, there times when it is clinically necessary to strengthen the Posterior Tibialis muscle and we like the following exercises

1. Single Leg Balance with Arch Supports:
Begin standing on one foot. Attempt to raise the medial longitudinal arch and hold in tact while maintaining the body stable over the foot.
2. Single Leg Balance with Arm Swings
Perform the exercise above and add to it multi planar arm swings while maintaining medial arch integrity and balance. Cross body arm swings that generate torso rotation, and simulated axe and pitching motion with each arm are effective motions to use.
3. Seated Forefoot Adduction and Inversion
This exercises utilizes some sort of resistive device such as a theraband that will wrap around the forefoot to attach somewhere lateral to the body creating lateral resistance. while stabilizing the ipsilateral knee with the contralateral hand the exercise is performed by adducting the forefoot against resistance towards the midline.
4. Inverted Calf raises
This exercise is performed standing. it should be started as a double support exercise and can be transitioned into a single support for added challenge. the exercise is performed by performing a standard calf raise with or with out Y-axis resistance and adding an inverted moment at the apex of the raise and then lowering back down.
5. Closed Chain Unilateral Supination
Standing on one leg on a step with the knee slightly flexed and the medial border of the foot over the edge of the step. Exercise is performed by lowering and lifting the arch from pronation to supination.

6. Now perform the sequence with appropriate arch intergrity WITHOUT the arch supports

These exercises should get you started. Good luck and let us know if you have any other questions.

The Gait Guys

The Gait Guys: Some strategies in Controlling the Foot Arches and Big Toe

As promised. We fixed the volume.  Less hiss next time. Enjoy

Dr. Shawn Allen of The Gait Guys speaks about proper stabilization of the medial foot and arch. Muscle specifically discussed are a team: FHB (flexor hallucis brevis), AbDuctor hallucis, and tibialis posterior. He discusses the functional anatomy, normal and pathologic movement patterns of the arch and first ray complex and big toe (hallux). His foot’s ability to show the optimal patterns for the arch and hallux are excellent examples. Follow up videos and DVDs will show more details you need to know, and some of the exercises he and Dr. Ivo Waerlop use to restore a foot that has lost these abilities. The DVDs are in the works. Take their lectures and CME on www.onlineCE.com. Visit them at www.thegaitguys.com and on their facebook PAGE & Twitter of the same name for daily feeds of unique things.