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Medial tibial stress syndrome

Discussion in 'Biomechanics, Sports and Foot orthoses' started by admin, Apr 1, 2006.

  1. admin

    admin Administrator Staff Member

    Members do not see these Ads. Sign Up.
    I think we need a thread on this for no other reason than the 'behind the scenes' logs tell me that a number of people type this into the search box looking for information on MTSS and we have no information on it :)

    Anyone want to share their pearls?
  2. Admin2

    Admin2 Administrator Staff Member

  3. Last October, I was invited as keynote podiatric speaker at the 2005 Australian Conference of Science and Medicine in Sport in Melbourne, Australia. The title of one of my lectures was "Medial Tibial Stress Syndrome: Biomechanical Etiology and Effective Foot Orthosis Treatment". As follows is an outline of my lecture.

  4. Craig Payne

    Craig Payne Moderator

    Me thinks this is a good course of enquiry for research on MTTS:
    I seem to recall a FEM model of tibia that showed greatest bending moments in tibia occur at the same spot that most get MTSS symptoms.

  5. Both Beck's and Milgrom's research seem to indicate that bending moments on tibia are a likely cause of medial tibial stress syndrome (MTSS). Certainly, any engineer will tell you that the bending stresses in a beam under bending load will be greatest at the narrowest narrow section of the beam. The area that seems to get the most tibial stress fractures and MTSS is at the narrowest section of the tibia (junction of proximal 2/3rds and distal 1/3rd).

    However, I tend to think that both bending moments and traction on soleal fascia, or other muscular structures such as the flexor digitorum longus, are the most likely causes of vast majority of MTSS cases. Both bending moments and medial fascial/muscular traction will tend to respond to varus rearfoot and forefoot wedged orthoses since these orthoses will shift the center of pressure more medially on the foot.
  6. gold

    gold Member

    I have recently seen a number of patients whom hyave had MTSS. These patients all seem to have had a similar foot structure. inverted rearfoot position and slightly valgus forefoot. The other factor o note is also the tibail varus. slightly tight posterior muscle compartment. I am wondering if in these patients is tibial bending that is causing the problem. I guess we can also assume that a lateral CofP due to tibial varus is also contributing. Now surely you wouldnt be considering a ff varus extension for these patients?
  7. If a runner has a "slight valgus forefoot" of, let's say, 2 degrees, and an "inverted rearfoot position" so that in relaxed calcaneal stance position they are found to be 3 degrees inverted and, at the maximally pronated subtalar joint (STJ) position can pronate to the heel vertical position only, then you are saying that we should not use a forefoot varus extension on the orthosis to treat medial tibial stress syndrome (MTSS)? Right??

    People don't get MTSS from walking, it occurs from running. It probably occurs due to excessive lateral positioning of the center of pressure (CoP) during the first half of stance phase of running. As you will rembember, running is not just an accelerated form of walking. Running and walking are two very different activities that are, in some cases, diametrically opposed to each other biomechanically.

    In running (not jogging), the decreased base of gait caused by running limb varus will take our runner above with a "inverted rearfoot and slight valgus forefoot" to a position of, on average, probably 5 degrees more inverted at the rearfoot and forefoot. So now, if we factor in the 5 degrees of running limb varus, the runner will effectively have their heel inverted 5 degrees when their STJ is maximally pronated during running. Now that 2 degrees of forefoot valgus becomes probably more like a 3 degree inverted forefoot to ground relationship, if the STJ is maximally pronated, and will be even in more varus to the ground if the STJ is supinated from the maximally pronated STJ position. Since the medial column will dorsiflex more under load than the lateral column, then effectively, the CoP will indeed be quite lateral in your runner that has an "inverted rearfoot and slight valgus forefoot".

    In this runner, I would use a forefoot varus extension not only because it makes better biomechanical sense but because, in 20+ years of treating these runners, that is what works best as a forefoot extension on their inverted foot orthoses. Forget about what you measure using the Root et al techniques. Orient the foot and lower extremities in the running position on the table, position the STJ in the neutral position, load both the medial and lateral forefoot and then see if the forefoot is in a valgus or varus position relative to their transverse plane. I think that you will find that nearly all your MTSS patients with a "slight valgus forefoot" now have a varus forefoot to ground relationship.
  8. gold

    gold Member

    Sorry I may be be slightly ignorant here but please fill me in on whether or not these forefoot varus wedge extensions will have an effect on windlass mechanics. Will these wedge extensions place a dorsiflexion force through the head of the first met? Thus increasing the force required to activate the windlass?
  9. Craig Payne

    Craig Payne Moderator

    You are right about it possibly interfering with windlass mechanics. Kevin and I had this discussion when he was down here last year. However, I tend to use a small varus wedge along the entire foot --- usually no more the 3-4mm, so:

    1) The rearfoot is inverted as well with the wedge, which has a positive effect on windlass mechanics
    2) As its used for running, the so called 'runners varus' comes into play due to narrower base of gait during running - this will have the effect of lessening the possibility of interfering with windlass mechanics.

    Since talking with Kevin about this, I have the protocol for an experiment in place to investigate its effects on windlass mechanics ... just have not got to yet .... I have to keep reminding myself that "students are the reason for my work and not an interuption to my work"
  10. gold

    gold Member

    thanks for the help craig.
  11. As Craig and I have said, running and walking mechanics are quite different. In walking, the individual gradually loads the forefoot and then pushes off the forefoot. In running, the time spent in the whole stance (i.e. support) phase is about 250 ms so that there is more of a rapid "jumping motion" off from one foot to another. This is better appreciated by watching slow motion video of an individual's foot both walking and running....there is quite a difference.

    For those patients with MTSS, the thickness of the varus forefoot extension under the first metatarsal head is usually around 3 mm, ground so that it tapers gradually laterally to where it will then end between the 4th and 5th metatarsal. However, I have had to make the varus forefoot extension sometimes up to 6 mm thick at the first metatarsal head for some runners, but this is rare.

    The varus forefoot extension is always combined with an orthosis that is inverted about 5-7 degrees, has a rearfoot post, a medial heel skive of 2-6 mm and is made with a shell material that will deform only about 2-3 mm in the medial arch when loaded by the runner during the middle of midstance. I use either plastazote #3 or 5/32" or 3/16" polypropylene most commonly as an orthosis shell material for these runner's orthoses.

    I tell my patients that these varus forefoot extension orthoses have been "tuned" specifically for running and should not be used for walking since I am worried about potential problems with first ray/first MPJ mechanics in walking with large amounts of varus forefoot extensions. I don't worry about this being a factor in running since the requirements for first MPJ dorsiflexion seem to be much less for running than for walking and I don't think the windlass is as big of a factor for running as it is for walking.

    The effect of forefoot varus extensions in treating MTSS is huge, not minimal. You will get a much higher success rate of treating MTSS with forefoot varus extensions in orthoses than you will ever get without this orthosis modification.

    Also, one more thing, since many of these runners tend to be forefoot strikers, I put them on gastroc-soleus stretches three times a day and try to raise the heel of the orthosis so that they become more of a midfoot-rearfoot striker. This will significantly shift the CoP medially to being more in line with the longitudinal axis of the tibia at footstrike so that tibial bending moments are minimized.
  12. NewsBot

    NewsBot The Admin that posts the news.

    Exercise-Related Leg Pain in Female Collegiate Athletes: The Influence of Intrinsic and Extrinsic Factors.
    Am J Sports Med. 2006 Apr 24;
  13. Stanley

    Stanley Well-Known Member

    Just a few tips on this condition.

    Diagnosis: The pain is at the myo-tendinous junction of the posterior tibial. Palpate the tender area (about 12cm proximal to the medial malleolus, just posterior to the medial tibial border), and have the patient maximally contract the posterior tibial muscle. If the PT is the affected muscle, the pain will increase. The stress fracture associated with the weakness of this muscle is on the anterior medial portion of the calcaneus. The posterior tibial muscle prevents eccentric loading of the tibial. When the muscle is damaged, it cannot maintain concentric loading.
    1. Make an orthosis that corrects for varus imbalance in the rearfoot. Also grind out sub 1 to eliminate propulsive pronation. Use heel lifts appropriately for the leg length and equinus.
    2. Physical therapy consisting of ultrasound and massage (superficial pettrisage) at the area of the myotendionus junction. The pettrisage is effective especially in the chronic cases. When you pinch the soft tissue above the painful area is should bulge between your finger tips. If it doesn't it needs the pettrisage.
    3. Strengthening of the posterior tibial muscle. Stretch the gastrocs.
    4. Shoe modification: Grind the midsole in the lateral heel area to soften the lateral heel, which is a pronatory lever at heel contact.
    5. Taping: I published a taping in Physician and Sports Medicine in 1982, which is an assist taping for the posterior tibial. Three strips of 1" elastoplast under tension are used to duplicate the posterior tibial muscle. If you find the article it will say Elastikon. This was changed by Physician and Sports Medicine to appease their advertiser. By the way, this taping I use in cases of tibial stress fractures related to weakness of the posterior tibial muscle. I tape the patient and have them walk 3 miles per day for two weeks, and then have them run with the taping for two more weeks to tolerance. I tell them if they get worse to D/C the running, but this rarely occurs.
    6. Manipulation: Cuneifoms can be plantar medial. The Hiss manipulation works well for these. (Remember that the PT inserts into the cuneiforms, and if the joint is subluxed plantarly, contraction of the PT will pull the joint more into deformity) For the Equinus, fibular manipulations can be helpful. Also check the navicular and talus.
    7. Cranial sacral work can be extremely helpful. I have noticed that orthodontic appliances will result in weak posterior tibial muscles, as it binds the skull. In these cases, the results can be limited until after the appliance is removed and the cranial work is performed. The Universal
    interosseous Cranial Fault, Jamming of the Cruciate and Sagittal sutures are very common, but not all that can occur. Sometimes just this correction (when applicable) will eliminate the weakness of the posterior tibial muscle, the equinus and the apparent leg length.
    I once lectured at a Road Running Club and I said that PT shin splints (the old term for Medial tibial stress syndrome) was caused by weak PT muscles. A runner came up to me afterwards and asked "Doc, I run every day and have shinsplints, why are my muscles weak? An excellent question whose answer can only be explained by a neurologic mechanism.

  14. N.N.

    N.N. Member

    Long time reader first time poster.
    I was reading through this informative thread, and understood everything that was posted, until I was a bit stumped on this suggestion posted by Stanley.
    Are there any articles that explain this, as I didn't have any luck finding any relevant information, and I don't quite understand relationship of the UICF to Post. Tib. muscle weakness.

  15. Stanley

    Stanley Well-Known Member


    I have learned this information by taking courses in Applied Kinesiology, and applying it to the lower extremity. I will ask for references.

  16. We now know that the posterior tibial muscle is not the most likely cause of medial tibial stress syndrome. It is more likely caused by fascial attachments of the soleus, the origin of the flexor digitorum longus or by valgus bending moments on the tibia. The posterior tibial muscle has been shown in numerous studies to not originate along the medial border of the tibia. So to say it is caused by the posterior tibial muscle is simply not supported by the best evidence to date.

    Also, just because a runner is active daily in training does not mean that all their muscles are strong. Muscles may be intrinsically strong (i.e. large cross-sectional diameter) but may have a shortened moment arm, thus making them function as weak muscles.

    For example, the normal foot may have a posterior tibial tendon that has a 30 mm supination moment arm to the subtalar joint (STJ) axis. However, a foot with a severely medially deviated STJ axis may have only a 5 mm supination moment arm to the STJ axis. Therefore, even though the normal foot and the medially deviated STJ axis foot may have posterior tibial muscles which have the exact same absolute strength, the foot with the normal STJ axis will be perceived by the examiner to be 6 times stronger than the posterior tibial muscle in the medially deviated STJ axis foot. This then provides a mechanically coherent explanation how an individual may exercise daily but still possess a mechanically inefficient or "weak" muscle. In other words, this phenomenon can easily be explained by a non-neurological mechanism.
  17. Stanley

    Stanley Well-Known Member

    I haven't read the studies, but all you have to do is to palpate the painful area and have the patient supinate the foot maximally to contract the posterior tibial muscle FULLY, and you will find out very quickly that it is not caused by fascial attachments of the soleus, the origin of the flexor digitorum longus or by valgus bending moments on the tibia. As far as the valgus bending moments of the tibia, they are there but are neutralized by the posterior tibial muscle. This is called concentric loading. When the posterior tibial muscle fails to neutralize the bending moments, motion occurs and there is another condition that develops called a stress fracture. This is a result of eccentric loading. As far as the Flexor digitorum longus muscle is concerned, you can get shin splints related to this, but they are higher on the leg, and the pain is reproduced by flexion of the digits. This muscle stops bending moments in the proximal third of the tibia. I am surprised you didn't mention the flexor hallucis longus, as this can also cause shin splints lower down than the posterior tibial muscle.
    Sometimes the fascia around the posterior tibia is bound down, and superficial petrissage helps, but this is in the more chronic cases.
    Regarding the neurologic reason for muscle development, if a muscle does not contract fully, it will not get stonger. The test for this is to see if the muscle summates (locks). If it does, then it has the capacity to strengthen. If it doesn't, it is prone to injury.
    I have changed the moments on the posterior tibial muscle by modifiying the lateral flanges of shoes and making orthotics, and yes this helps. But my results are much better by getting the posterior tibial muscles to function normally.
  18. Phil Wells

    Phil Wells Active Member

    Kevin and Craig
    This question may be 'chewing over old soup, but why use any rearfoot posting/control on the running foot?
    I understand that it will effect the orthoses mechanics structurally, will have an effect when the person is walking etc but when running the heel/orthoses GRF may be very minimal.
    Are we talking about pre-positioning of the heel or other?

    Sorry about this one but I have good results with these groups when rear foot posts are used but I am not sure whether they are changing the STj location or modifying sagital plane function - heel raise.

  19. Stanley:

    Even though I appreciate your clinical fervor, it would behoove you to take the time to read the current studies on medial tibial stress syndrome (MTSS) and tibial stress fracture since you would then discover that your conjectures above simply are not supported in the literature.

    First of all, all authors except for Saxena do not believe that the posterior tibial muscle could possibly be the cause of MTSS since the posterior tibial does not originate from the medial tibial border:

    Saxena A, O’Brien T, Bunce D: Anatomic dissection of the tibialis posterior muscle and its correlation to medial tibial stress syndrome. J Foot Surg, 29:105-108, 1990.

    Detmer DE: Chronic shin splints: Classification and management of medial tibial stress syndrome. Am J Sp Med, 3:436-446, 1986.

    Michael RH, Holder LE: The soleus syndrome. A cause of medial tibial stress (shin splints). Am J Sp Med, 13:87-94, 1985.

    Garth WP, Miller STJ: Evaluation of claw toe deformity, weakness of foot intrinsics, and posteromedial shin pain. Am J Sp Med, 17:821-827, 1989.

    Beck BR, Osternig LR: Medial tibial stress syndrome: The location of muscles in the leg in relation to symptoms. JBJS, 76A:1057-1061, 1994.

    Secondly, bending of the tibia is now thought to possibly be a primary cause of both MTSS and tibial stress fracture:

    Milgrom C, Giladi M, Simkin A, et al: The area moment of inertia of the tibia: A risk factor for stress fractures. J. Biomech, 21:1243-1248, 1989.

    Beck TJ, Ruff CB, Mourtnda FA, et al: Dual-energy x-ray absorptiometry derived structural geometry for stress fracture prediction in male US Marine Corp recruits. J Bone Miner Res, 11:645-653, 1996.

    Beck BR: Tibial stress injuries: An aetiological review for purposes of guiding management. Sports Med, 26:265-279, 1998.

    It is my belief that bending of the tibia may cause the majority of MTSS and tibial stress fractures due to the combination of the following factors:

    1. Eccentric loading of the tibia caused by the ground reaction force vector being laterally located relative to the long axis of the tibia at footstrike during running.

    2. Decreased bone density in the tibia.

    3. Decreased area moment of inertia of the tibia that increases magnitude of bending stresses at this section of the tibia. http://www.tamu.edu/classes/cosc/nichols/classes/structuralsystems1/handouts/ho21eccentricity.pdf#search='eccentric%20loading'

    You can read my lecture I gave in Melbourne last year (at the beginning of this thread) that gives a more complete overview of MTSS and tibial stress fracture.
  20. Stanley

    Stanley Well-Known Member


    Thanks for the references. I reviewed the abstracts and this is what I found:
    Saxena’s article was looking for the origin of the posterior tibial muscle, and he did not find it in the area of the lower third of the tibia. This only means that the origin of the muscle is not involved, and I agree with this.
    Detmer started with the 3 possibilities of tibial pain (which were stress fracture, periostitis, or compartment syndrome)and then he classified the 3 as type I, II (periostalgia from chronic avulsion of the periosteum at the periosteal-fascial junction), and III. He took chronic cases and operated on type II and III. These were chronic cases that do develop adhesions. He performed a fasciotomy and performed cauterization of the periosteum. So he implies the fascia is involved, and it is in chronic cases, so I agree.
    Michael’s article shows increase uptake on the tibia, he found the increased activity is related to periostitis and new bone activity (on 1 live patient). The soleus is implicated in causing these changes. I agree that there is bony adaptation to stress that can occur due to eccentric loading. 1 live patient is not enough to say that pain in this region on all patients is related to periostitis.
    Garth’s article found in symptomatic patients, a significant displacement of the arc of motion of the second toe in the symptomatic athletes toward extension of the metatarsophalangeal joint and a decrease in flexion. Weakness or dysfunction of the intrinsic muscles in the symptomatic athletes was also found to be significant. This analysis supports the hypothesis that posteromedial middle one-third tibial stress symptoms may be related to overuse of the flexor digitorum longus muscle associated with mild claw toe deformity.
    Beck found the soleus, the flexor digitorum longus, and the deep crural fascia were found to attach most frequently at the site where symptoms of medial tibial stress syndrome occur, while in no specimen was the tibialis posterior found to attach at this site. I agree that the origin of the posterior tibial muscle is not involved.
    I read the primer on eccentric/concentric loading. I would appreciate an explanation of the calculus, as this is the only thing I didn’t fully understand.
    You mention that current thinking is based on these articles. I found there was only one that was less than 10 years old, so I can use some much older stuff than this in the discussion.
    It was Dick Schuster that lectured in 1976 that the posterior shin splint was a pre stress fracture, and I remember him actually duplicating the pain by bending the tibia using his knee and two hands.
    I found this true in some cases, and it stumped me as to what was going on. By accident I found that full contraction of the posterior tibial muscle (supination of the foot) would increase the pain of palpation. Since there is no other explanation, than this is related to the posterior tibial muscle, we have to ask what structures are involved with the pain. The only possible answer is the myo-tendinous junction of the posterior tibial muscle, and the fascia related to it.
    In the first few pages of Steindler’s Kinesiology book you will find that one of the functions of muscles is to change eccentric loading of bone and convert it to concentric loading. Failure of the muscle will allow for eccentric loading. Theoretically then if you were to assist the muscle and help to convert eccentric loading, then you can stabilize bone and eliminate pain. This is exactly what happens with a posterior tibial assist tape (I published this in the early 80’s in Physician and Sports Medicine). Put the tape on and the stress fracture patient can jump up and down.
    So to summarize, the posterior tibial muscle is involved with concentric loading of the tibia. Failure of the muscle results in pain initially at the myo-tendinous junction, followed by the fascia and its connection to the periosteum, and finally due to eccentric loading the bone fractures. Early treatment should be directed at preventing failure of the posterior tibial muscle by taping, orthotics, modifying shoes, and by decreasing dysponesis,
    I hope this helps you properly interpret the articles you quoted.


  21. Stanley:

    Even though your conjectures above are the same ones that I have heard, for many years, from other clinicians who are not familiar with the literature on this subject, your ideas don't make much sense from the hundreds of patients I have examined and treated with this condition or from review of the literature. If the pain of MTSS is caused by damage at the myo-tendinous junction of the posterior tibial muscle, then how does this explain the positive bone scan and MRI findings (i.e. periosteal edema and bone marrow edema) within the medial border of the tibia, where most of the patients are tender with MTSS? In addition, in all the patients I have examined with MTSS, active resistance testing of the posterior tibial muscle has not reproduced the symptoms in these patients. If MTSS is a "myo-tendinous junction" injury of the posterior tibial muscle, why doesn't an increase in tensile stress in the muscle/tendon cause increased symptoms?
    Last edited: Aug 4, 2006
  22. Stanley

    Stanley Well-Known Member


    I explained this in my prior post, I guess I wasn’t clear enough. :eek:

    “In the first few pages of Steindler’s Kinesiology book you will find that one of the functions of muscles is to change eccentric loading of bone and convert it to concentric loading. Failure of the muscle will allow for eccentric loading. Theoretically then if you were to assist the muscle and help to convert eccentric loading, then you can stabilize bone and eliminate pain. This is exactly what happens with a posterior tibial assist tape (I published this in the early 80’s in Physician and Sports Medicine). Put the tape on and the stress fracture patient can jump up and down.
    So to summarize, the posterior tibial muscle is involved with concentric loading of the tibia. Failure of the muscle results in pain initially at the myo-tendinous junction, followed by the fascia and its connection to the periosteum, and finally due to eccentric loading the bone fractures”

    When the muscle fails the bone develops eccentric loading. Depending on what the patient does next, either the tibia adapts or it fails. Different muscles stabilize different areas of bone (usually posterior tibial for the distal 1/3, usually flexor digitorum longus for the proximal 1/3), In either case you would get bony changes as seen on the MRI and bone scan. By the way a few years ago I lectured on taping to convert eccentric loading to concentric loading for the treatment of stress fractures. I only discussed 5 muscles/tapings/stress fractures, as I don't know all of them yet.
    I think one of our differences is that you are looking at the beginning (valgus stress on the tibia) and end result (bone changes) while I am cognizant of this, but am focusing on the bodies mechanism that protects the bone. One of the questions is what exactly hurts, bone, periosteum, muscle, or fascia.
    In 1978, I developed shin splints due to overtraining (Going from 0-10 miles miles/week week 1 and then going to 15 miles/week week 2). I wanted to run a marathon in 6 months. The pain got worse, since I knew it was the posterior tibial muscle (after treating it in hundreds of patients), I developed an assist tape for it. I wore the tape and used counter-irritants, and it allowed me to train. As scheduled, I ran the NYC marathon with the taping, and besides developing severe blisters on my leg, the pain from the shin splints was eliminated. If you could give me a better explanation than breaking down adhesions in the fascia, I would appreciate it.
    The key thing to testing the posterior tibial muscle is with CONTRACTION AT THE END RANGE OF ADDUCTION AGAINST RESISTANCE. This does not duplicate the pain in every case, as this can be caused by different muscles. This does apply to pain approximately 14 cm proximal to the medial malleolus.
    Could you also explain to me what is the body's mechanism to convert eccentric loading to concentric loading as written in Steindler's book? If not muscles then what? In the case of the lower tibia, if not the posterior tibial muscle, then which one has failed to function properly?
    By the way, thanks for the references. I had a patient that had atypical shin splints yesterday. His pain was mid tibia (posterior medial border) that was not increased by adduction or digital plantarflexion. It was however increased by plantarflexion of the ankle. So I guess this one is related to the soleus. :eek:
    I just noticed your post of your lecture Medial Tibial Stress Syndrome: Biomechanical Etiology and Effective Foot Orthosis Treatment. It looks very comprehensive. It will take me time to digest it.


  23. Here is a paper that I thought may be of interest to this discussion:

  24. Stanley

    Stanley Well-Known Member


    Nice article, but I think we already know the point it is making regarding the valgus moment in the tibia.
    By the way I had some time to review your excellent presentation on shin splints.
    Just a few things hit me as contradictory.
    You have tibia varum listed as an etiology. Wouldn't this decrease the valgus moment on the tibia by moving the CoP medially?
    Viitasalo and also Bennett showed navicular drop, and this is related to pronation. Pronation would fatigue the posterior tibial muscle, so this correlates with posterior tibial muscle weakness.
    In your summary you say:
    Likely etiologies of MTSS include increased tensile forces from medial tibial muscles/fascia and increased valgus bending moment on tibia during running and jumping activities
    A muscle medial to the tibia should cause a varus bending moment on the tibia to neutralize or diminish the valgus bending moments caused by running and jumping.
    Bouche and Johnson see ..... an increase in visible bowstringing and measured strain in the medial tibial fascia with tensile loads applied to all three muscles....(PT, FDL, and Soleus). It is very interesting to note that the PT is listed in the three muscles he tested. So the function of fascia and muscles that insert on it (due to its location) is designed to convert eccentric loading to concentric loading. This is why I think that the failure of any of these muscle would cause the valgus bending moment. I also do not think it is unreasonable to think that each muscle would cause a different moment, and therefore stabilize a different portion of the tibia, and the posterior tibial muscle appears to be the muscle that stabilizes the lower third of the tibia (by virtue of the results of the assist taping).


  25. It is my opinion that increased tibial varum would cause the center of pressure (CoP) to be shifted laterally at footstrike during running since the lateral rearfoot and/or forefoot would become the predominant loading point on the plantar foot during contact phase. Increased lateral CoP positioning would, in turn, increase the eccentric load (i.e. non-axial load) on the tibia during contact and early support phase of running. This would, in turn, increase the valgus bending moment on the tibia and increase the likelihood that microfractures may develop in the medial tibia which would, in time, cause medial tibial stress syndrome (MTSS)/medial tibial stress fracture (MTSF) to possibly result.

    I am not so sure that contractile activity of any of the leg muscles would have much effect on the bending moments on the tibia since all of these muscles originate fairly much in line with the long axis of the tibia. They would have a much stronger mechanical effect to cause a varus tibial bending moment if they originated from the medial femoral epicondyle and attached to the medial foot. In other words, the characteristic human structural arrangement in the leg of axially oriented muscles trying to counterbalance non-axial loading forces due to lateral CoP positioning at foot strike during running will naturally cause increased bending moments on the tibia and increase the likelihood of MTSS and MTSF.

    The data from Bouche comes from Richard Bouche, DPM from Seattle. Rich sent me his experimental photos and preliminary experimental results since he has been thinking and working on MTSS for years. He likes to call MTSS "tibial fasciitis" since he thinks the disease is due primarily to tensile forces on the deep compartment fascia and soleus fascia that attach along the medial tibial border.

    I think that Rich is partially right and I would have to agree with you, Stanley, that the posterior tibial muscle could possibly play some role. However, so far the literature is focusing more on bending moments and the other muscles in that area that have stronger attachments at the medial tibial border. When I did the extensive literature review for MTSS for my Melbourne lecture, my thinking about MTSS and MTSF changed quite a bit. Stanley, I think you would be very interested in the MRI study and histology studies I listed in my lecture since both seem to point to MTSS being a possible precursor or early stage of MTSF. Fascinating stuff!
  26. Scorpio622

    Scorpio622 Active Member

  27. Nick,

    Look at the answer I gave Stanley a few postings ago in response to basically the same question:

    Here is one of the illustrations that I drew for the lecture that describes this mechanical effect...hope it helps.

    Attached Files:

  28. Stanley

    Stanley Well-Known Member


    It was a pleasure meeting you at the APMA meeting.
    I have to agree that the leg muscles would have a stronger effect if it originated further from the long axis of the tibia. This would necessitate a much thicker and heavier leg which would slow down running speed. There is a mechanism present to increase the strength, and that is eccentric contraction.
    What is interesting is you say that “the characteristic human structural arrangement in the leg of axially oriented muscles trying to counterbalance non-axial loading forces due to lateral CoP positioning at foot strike during running will naturally cause increased bending moments on the tibia and increase the likelihood of MTSS and MTSF”. If the muscles can increase lateral bending moments on the tibia, correctly placed muscles should be able to decrease these moments to the point where the stiffness of the bone should be able to handle them.
    The concept of “tibial fasciitis” is an interesting one. The question that this makes one ask is what is the purpose of the tension of the soleus (and also the PT and FDL) on the fascia? It makes sense that the fascial tension is to provide a moment to decrease the valgus bending moment on the tibia.
    Kevin, I agree that MTSS can become MTSF. This is due to failure to maintain concentric loading via failure of the muscles to provide a varus moment. It is precisely the failure of the muscles that will allow the eccentric loading. The bone will not break without this eccentric loading (which is the moments not being controlled by the leg).

    Regarding your diagram of the tibial varum causing a valgus moment on the tibia. You make an assumption that I am not sure is valid. You are assuming that the lateral forefoot is able to efficiently transmit the force up to the tibia. For this to occur, the subtalar joint would have to have a high level of stiffness. This stiffness would have to be provided by the posterior tibial muscle that as it contracts would provide a varus bending moment to the tibia. It is an interesting arrangement.


  29. Stanley, it was good to finally meet the man behind the name in Lost Wages.....uh...I mean Las Vegas. R. McNeill Alexander has done quite a bit of work on how different animal species have morphologic characteristics which are mechanically optimized for their survival in their particular environment. One of his books that I have read (and I have in my library)is "Optima for Animals" where he goes into great detail regarding these types of concepts (Alexander, R. McNeill: Optima for Animals. Princeton University Press, Princeton, New Jersey 1996).

    What I meant is that the ground reaction force causes the valgus bending moments on the tibia and the axially oriented muscles of the leg are not positioned optimally to resist these valgus bending moments. Individuals with thick tibias and good bone density can probably handle these valgus bending loads with no problem. The problem is that many female athletes have thin tibias and probably have lower bone density than their male counterparts and this probably explains their increased tendency to develop tibial stress fracture and MTSS.

    The soleal fascia attaches the soleus to the medial border of the tibia. Does this structure have a purpose other than to attach the soleus to the tibia???...I don't know.

    I am not sure that this all can be blamed on the muscles. MTSS and MTSF could also simply be due to a thin tibia that has decreased bone density being subjected to valgus bending moments with each running step....rather than weak muscles.

    This is a technique called quasi-static modelling. http://www.vard.org/jour/99/36/3/jacob.pdf Quasi-staic modelling assumes that the loads are transmitted up the leg from the foot just as if the foot and ankle and tibia were all one unit, which is obviously not the case. But in modelling, this is a valid and commonly used concept. However, quasi-static modelling only approximates the loads but certainly seems like a valid type of model to use in this type of analysis, especially since the force acting on the lateral forefoot at footstrike will instantaneously be transmitted to the tibia as bending moments which may ultimately cause MTSS and MTSF.

    By the way, I don't think the posterior tibial muscle has significant mechanical ability to cause a varus bending moment on the tibia since much of it originates posterior and lateral to the tibia. If the PT muscle could exert storng varus bending moments on the tibia, then there would probably be far fewer cases of MTSS and MTSF.

    Again, nice meeting you Stanley. Your contributions to this list are greatly appreciated.
    Last edited: Aug 12, 2006
  30. Stanley

    Stanley Well-Known Member

    Kevin, I agree that this is not the optimum arrangement. The reason I think that the muscles have an effect is 1. Steindler showing that muscles convert eccentric to concentric loading, and 2. Bones are like bricks-very good in resisting compression forces and poor in resisting tension forces. Bony adaptaton can only account for so much. Bone density helps with compression forces and diameter helps with tension forces ( the stiffness of a hollow tube is proportional to the third power of the radius). But even this doesn't account for the magnitude of the valgus bending moments. To calculate the moment we would take the distance of the weight bearing axis of the tibia to the CofP (approximately 1-1.5cm [Plato Schwartz wrote an article on this distance]) times the body weight times let us say 1.5. So in a 160 pound man, we are talking about the equivalence of 1/2" times 240 pounds or 5 pounds at 2 feet. So if we were to take an average tibia at 2 foot length and placed it in a clamp on one end and subjected it to a 5 pound weight for one thousand repititions every eight minutes, how long do you think it would take to fail? This is the exact force on the tibia in running an eight minute mile eliminating muscle and fascial factors.
    I read the article on modeling and it is a fascinating work. I am not sure this is the model that is best for what we are talking about. The modelling is limited by the complexity of the model. The modeling that was used in the article was very complex, but there was an instance in the model that was not taken into account. In Hanson's disease there is a neuropathy, and the reflex of the muscles to protect the joints is not intact. Another example if you have ever broken a board with your hand, you would know that you have to tighten the muscles maximally in your hand before striking the board. If you do not, then your hand will break. The moments produced by striking the board would be medial bending. There is nothing in the hand that would have a clear mechanical advantage to provide the lateral bending moments to counteract the medial bending moments generated by the strike. Bony adaptation does not explain the hand not breaking, as there is only so much adaptation that can take, place, and a relaxed hand would break. So this leads me to the tensegrity theory that Kevin Miller has talked about. An example of this is a geodesic dome. Any force applied to it is negated by the entire structure. I think that this model makes more sense.
    I was looking at the anatomy and higher up the leg the posterior tibial muscle cannot apply the force to resist the valgus bending moment, but it can further down the leg when the tendon goes more medially. It would appear that at the level of the midtibia, the Anterior tibial muscle is probably in a better position to resist the posterior and valgus tension where these stress fractures occur.
    This brings me to the point of we may be discussing two different stress fractures. I remember as a student listening to Subotnick and Schuster. One said the long side pronates and the other said the short side pronates. It took me years to figure out that they were seeing different types of patients (world class vs. weekend warriors). Putting together these differences allowed me to understand that the world class runners lengthen the short leg via equinus (and then get equinus compensations-pronation) and the weekend warriors shorten the long leg (pronation). I am thinking that you are talking about middle 1/3 stress fractures (which is more soleus related) and I am talking about lower 1/3 stress fractures (more posterior tibial related). The stress fractures I tend to see are in the anterior medial tibia. I have seen the posterior medial ones also, but much less often, and thought it was just a weird variation of the anterior medial one.
    I wanted to thank you for inviting me to join the Listserve, and from that Podiatry arena. You have made me take a hard look at what I was thinking about and I have changed several things in the last few years.
  31. NewsBot

    NewsBot The Admin that posts the news.

    Endurance of the ankle joint plantar flexor muscles in athletes with medial tibial stress syndrome: A case-control study.
    J Sci Med Sport. 2007 Feb 28;
    Madeley LT, Munteanu SE, Bonanno DR
    Last edited by a moderator: Mar 7, 2007
  32. Stanley

    Stanley Well-Known Member

    Excellent article. I have argued that weak muscles would cause MTSS by the fact it would change eccentric to concentric loading. I was wondering if there is a possible mechanism to explain the weak muscle as a result of MTSS.

  33. NewsBot

    NewsBot The Admin that posts the news.

    Medial tibial stress syndrome in high school cross-country runners: incidence and risk factors.
    Plisky MS, Rauh MJ, Heiderscheit B, Underwood FB, Tank RT.
    J Orthop Sports Phys Ther. 2007 Feb;37(2):40-7.
  34. Pigsney

    Pigsney Member

    Have seen a patient with shin pain. 17 year old girl who has a history of 6 knee operations, both knees, between the age of 11 and 16. Has been through rehab and now recently started playing sport (netball) for first time in a long while. The knee surgery was regarding the alignnment of the patellae.
    She has a pes planus foot type and tight gastrocsoleus complex. Have discussed calf stretching and footwear. I want to prescribe some orthoses for her but am a little hesitant about whether polypropolene will be to hard, due to the surgical history of the knee. I am thinking maybe full length Polypropolene device with a soft cushioning cover. From experience what do you think? Is a plastic device definitely a no no due to her knee history? Any ideas welcome. Thanks.
  35. Stanley

    Stanley Well-Known Member

    I think you have to change your focus when you look at a patient.

    It is not about what orthotic should be made, but rather what is going on biomechanically, and how can it be treated.

    Equinus will make both legs toe out from the foot upwards increasing the Q angle and making a patient prone to chondromalacia (the patella tracking problem) Here in the States when I first got involved in Sports Medicine, the orthopedic surgeons would take out the patella for this condition, so don't let the fact she had surgery scare you off. All it means is that the orthopedic surgeon doesn't understand the cause of the condition, so how could he fix it?

    Equinus will also cause shin splints, and it will also make orthotics intolerable. You are dealing with an extrinsic pronatory condition,and you cannot expect the orthotic to correct something that is not in the foot.

    We can correct four things between the foot and the ground: Leg length, equinus, Pronation, and Metatarsal heights. Do not limit yourself to just the pronation aspect. In this case measure your dorsiflexion and place the heel lifts that are appropriate on your orthotic.

    I don't mean to sound harsh, but for you to really succeed in sports medicine you have to use all the tools in the orthotic tool kit.

    Best regards,

  36. Pigsney

    Pigsney Member

    Excellent. Thanks. I must agree, I overlooked the equinus aspect of the orthoses in this case.
  37. Stanley

    Stanley Well-Known Member

    You are very welcome. By the way, all you need to do is add a heel lift to the orthotic until you can get the gastroc stretched out (stretching, manipulation of the ankle, night splints, &/or whatever other techniques there are).


  38. Asher

    Asher Well-Known Member

    I have a MTSS case (20yo female - hockey, volleyball and other sports) who gets bruising along the medial tibial border. She's sure that the bruising is a part of the 'shin splints'. She has suffered with MTSS for many years.

    I have had some success with arch supports and heel raises but spoke to her in an informal setting on the weekend and the pain and bruising is back again after only a few weeks relief. On reading Kevin's past posts, I think I'm going to try a varus FF extension next but I don't know what to make of the bruising.

    What's the story with MTSS and bruising - is it coincidental?

  39. NewsBot

    NewsBot The Admin that posts the news.

    Association Between Foot Type And Tibial Stress Injuries: A Systematic Review.
    Barnes A, Wheat J, Milner C.
    Br J Sports Med. 2007 Nov 5; [Epub ahead of print]
  40. Romeu Araujo

    Romeu Araujo Active Member

    Hi all,


    Female, 34 year old, MTSS, used to do long walks through forests. Extreme tenderness in soft tissues in lower leg (medial side mostly), plantar fascia and presented and lower leg edema. When she came to me had already been in a vascular surgeon who ruled out any kind of vascular pathology – he prescribed her compression socks (for the hole limb) and physiotherapy - she felt a little better (edema control), but nothing more. Allthis in her right leg. In the left one a "insignificant disconfort".

    After that, she arrived to me (after 3 months). I asked for a RX (negative), I thought in a MRI but the healthcare plan she has does not cover it…:bang:
    I’ve applied ortothics (I do not prescribe – I do it…) with a rear foot varus post, an heel raise (“functional equinus”); stretching is being done. She improved a lot immediately and then slowly - not as much as I wanted. She’s doing now anti-inflammatory therapy.

    She cannot stop her job for a few weeks – will be fired – she works all day standing and sometimes does repetitive movements in a machine pedal…

    One of these days she walked for 45m and the pain got worse. She also refers that she feels better with the compression socks.

    Any suggestions? Some specific physiotherapy treatment, anti-inflammatory therapy, in water exercising?
    I apologize for my English – I hope I haven’t been too confusing…

    My best regards to you all from a long time reader,

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