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Tissue Stress Theory

Discussion in 'Biomechanics, Sports and Foot orthoses' started by Asher, Apr 21, 2009.

  1. Asher

    Asher Well-Known Member

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    Hi all, I have an issue with the tissue stress theory that I'm hoping Podiatry Arena (PA) can help me get my head around.

    My understanding of the tissue stress theory is that you identify the structure that is painful (or under stress) and provide a treatment that reduces the stress on that structure until it becomes asymptomatic.

    This is easy when something is painful, you can tinker with your intervention (lets say an orthosis) and once its not painful you have been sucessful.

    But some bony deformities are not painful so you don't have 'pain' to guide you as to when you have done enough. So I would be thinking that you would aim for some sort of kinematic or kinetic ideal. But my readings from PA suggest that it is difficult to define an ideal to aim for.

    So when applying the tissue stress theory to an asymptomatic bony deformity, for example HAV, you provide an orthosis with prescription variables to reduce stress on the structures of the first ray. But this can be done to varying degrees. How do you know which degree to stop at?


  2. Atlas

    Atlas Well-Known Member

    This is the best post I have read on PA for some time.

    If I had to pick one podiatric theory (and I cherry pick BTW) the tissue stress is the one.

    I think you have made me think that the tissue stress theory should be merged with Craig's windlass style testing. Get the patient with HAV to stand on an orthotic. Try to correct the HAV deformity. Note the resistance and difficulty to correct. Then add a FF valgus wedge for instance. Retest. That will guide you.

    Physiotherapist (Masters) & Podiatrist
  3. Craig Payne

    Craig Payne Moderator

    I am starting to change my thinking on some of this...

    There is a difference between an underpinning foot function/orthotic theory and an orthotic prescribing protocol ... and I think we have in the past confused the two.

    There are underpinning theories:
    - Traditional (Root) theory
    - Sagittal plane theory
    - Bojssen-Mollors axes
    - Sensory input theories
    - Reduction of kinetic parameters (I used to call this tissue stress theory)
    - Joint equilibrium theories (eg SALRE; the equilibrium about the MTJ)
    - etc

    And then there are prescription protocols:
    - foot typing approaches
    - pathology specific presribing
    - (the practical application of some of the above theories)

    Tissue stress theory is an interesting one, as is it really a theory? Does it encompass all the other theories? Is it really just good commensense clinical practice? (eg: under Root theorey tissue stress is reduced by dealing with the deviations from the biophysical criteria of normalcy; under sagittal plane theory, tissue stress is reduced by preventing the compensations that occur of one of the 3 pivots are blocked; etc etc)

    To answer your question:
    We don't know. Under tissue stress theory the aim is to reduce the forces that are causing tissue damage to a level below which that damage occurs (this also refers to foot orthotic function as well as daily and sporting activities). In your eg, we want to reduce the forces below the level that may be causing the bony abnormality (assuming that is what is causing the bony abnormality). Apart from what Ron mentioned, there are no real ways to determine exactly how far forces need to be reduced in the absense of painful symptoms. HOWEVER, maybe you just reduce forces as low as you can, as we have no information if lowering the forces "too" low is pathologic (except in the instances where this may affect stiffness in other structures)
  4. Rebecca:

    Tissue stress theory dictates that the clinician should focus on reducing the abnormal tissue stress levels on the injured structures with their mechanical methods of therapy. This involves using mechanical models of the foot where one understands, from the models, which tissue is receiving what types of stress, so that a proper mechanical treatment may be designed to reduce stress on the injured tissue without causing injury elsewhere.

    One could also use the same tissue stress modelling concepts when trying to devise a mechanical means to treat an asymptomic hallux abducto valgus (HAV) deformity conservatively via mechanical means. Therefore, in the example of HAV deformity, any therapy that reduces the first ray adduction moment and reduces the hallux abduction moment will aid in reducing the development of HAV. This may include 1st interdigital spacer pads, night splints, and foot orthoses that reduce the ground reaction force on the first ray during late midstance.

    Eric Fuller and I wrote a chapter called "Subtalar Joint Equilibrium and Tissue Stress Approach to Biomechanical Therapy of the Foot and Lower Extremity" over four years ago and we are hoping it will be published this year. Our chapter is a comprehensive description of the tissue stress approach of mechanical foot therapy using the STJ axis location/rotational equilibrium theory as the underpinning theory of how the foot functions under loading from both external and internal forces. I know you will enjoy it. Eric Fuller also published a nice article on first ray mechanics which we used in our chapter to explain hallux valgus deformity (Fuller, Eric A: The windlass mechanism of the foot: A mechanical model to explain pathology. JAPMA, 90:35-46, 2000). Our chapter should be seeing the light of day by the end of the year....or so we have been told.

    Tissue stress theory and subtalar joint axis location/rotational equilibrium theory work hand in hand to allow the clinician to better understand how to design optimal foot orthoses for their patients.
  5. Asher

    Asher Well-Known Member

    Thankyou for the replies thus far, they are very helpful. However, I would like to ask the same question but remove the words "tissue stress theory".

    If I am treating pain, I might provide an orthotic device with certain prescription variables. If it does not get rid of the pain, I will likely change or increase those prescription variables (eg: thicker forefoot valgus extension) until the pain goes away.

    But when it comes to bony deformities that are not painful, I can't be guided by the lack of symptoms to tell me I have done enough with the orthosis. This would be fine if there was a kinematic or kinetic ideal to aim for. Is there? If there isn't, where do I stop?


  6. pod29

    pod29 Active Member

    Hi Rebecca

    This may seem a little too simplified, but in the absence of higher technologies ( video, pedar etc ) to show changes in function, I think one of the best clinical indicators of orthoses function and effect has got to be comfort. Patient feedback will play a huge role in how I modify or manage orthotic therapy. You have qualitative tests such as Jacks and resupination resistance tests to assess the changes your orthoses are having mechanically, but I usually find that if the orthotic feels right, it usually is! Barring the odd occasion when the patient will walk into the clinic saying how fantastic their orthoses are, only for me to discover that they are in the wrong shoes!!!;)


  7. efuller

    efuller MVP

    The beginning of the theory is that tissues are damaged when placed under too much stress. (In short, things break. Stress causes them to break.) I also like to think in terms of a break down rate and a healing rate. A certain amount of repetitive stress will cause a certain amount of damage. A certain amount of damage will be healed in time. If the damage rate exceeds the healing rate there will be tissue failure, or a lot more pain. Stress reduction will allow the structure to heal. You may not need the same amount of stress reduction once it is healed.

    When to stop? If you go too far with your intervention you can cause problems. Too much valgus wedge can cause sinus tarsi pain or lateral column overload. Too much varus wedge effect in the heel can cause peroneal tendonitis. I've done both in my own orthotics. I didn't add a reverse Morton's extension to my orthotics till about 4 years ago. I wish I had done that much earlier. I still don't use a reverse Morton's extension in my dress shoes. It's a little too tight.

    If you had infinite time to try multiple adjustments then you could tweak the device and come up with a different orthotic for different occasions or different shoes.

    First, do no harm,

  8. Griff

    Griff Moderator


    If it is asymptomatic then what are you prescribing the orthoses for? In my opinion if there is no pain it is difficult to apply 'tissue stress theory' - we cannot 'see' tissue stress/kinetic parameters and therefore pain is often our only guide (in a clinical setting)

    Just my thoughts

    Last edited: Apr 21, 2009
  9. Atlas

    Atlas Well-Known Member


    what happens when patient "a" hobbles in with a medially orientated STJ axis...hard supination resistance test....pes pancakus etc...but has chronic lateral ankle instablility (aka lateral ankle tensile issue)?

    Physiotherapist (Masters) & Podiatrist
  10. Asher

    Asher Well-Known Member

    Are you saying that you wouldn't prescribe an orthosis for asymptomatic HAV, knowing that it is a progressive deformity?
  11. Griff

    Griff Moderator

    I'm saying there is very little evidence to suggest orthoses will prevent deterioration...infact I'm sure there was one study which showed orthoses can make things worse...(I'm sure Simon will join in soon and can correct me if my memory has failed me)

    I certainly would not prescribe an orthoses and tell patients it will prevent further deterioration, as I dont think its a promise we can make (however I am not saying I never prescribe them for HAV of course!)

    I suppose my point was that when considering tissue stress theory and its application to a patient then irrespective of visual appearance/alignment if there is no pain should we intervene? Should we be thinking forces and not motion? (Obviously I appreciate there are some grey areas though)
    Last edited: Apr 21, 2009
  12. Kenva

    Kenva Active Member

    I think that, as far as new theories concern, it is difficult to stick to only one set of mind. And perhaps we shouldn't, if we want to learn from 'mistakes' made in the past...
    For me, the insight in other possible approaches, was only opening up my window of vision and helping my clinical reasoning.
    I think the tissue stress approach in this particular situation is a difficult one to apply because there is no specific reference that you can 'measure', still you could use it if you think about it pure mechanically wise. Your therapy would perhaps not be a foot orthotic at onset but still you're applying the same model. Using the tissue stress approach goes beyond making foot orthotics...
    Even more, when you look at other models one could find that the sagital plane model can give another point of view and perhaps another insight in your therapeutic approach towards treating HAV...
  13. Ron:

    Chronic lateral ankle instability is multifactorial. It may be caused by a laterally deviated subtalar joint (STJ) axis. However, it may also be caused by previous partial or complete tears of the lateral ankle ligaments, weak peroneal muscles, by poor shoe gear or by performing certain activities. If I were to see a patient as you describe above, I would be looking for other causes of the chronic lateral ankle instability other than increased STJ supination moments coming from the spatial location of their STJ axis.
  14. Rebecca:

    Here are the goals of foot orthosis therapy that should guide you in treating each of your patients using tissue stress theory:

    1. Reduce the pathological forces that are causing the symptoms or deformity.
    2. Optimize gait function.
    3. Cause no other pathology or deformity to occur.

    Therefore, in your case of an asymptomatic "bony deformity", you would design the orthosis to reduce the pathological forces that would cause further progression of the bony deformity, you would also try to optimize the patient's gait function, but you would not add so much "correction" in the orthosis that another problem occurs. The application of these very simple goals of tissue stress theory should be applied to all patients receiving custom foot orthoses.
  15. In the case of hallux valgus, when progression is stopped, you know you've hit the nail on the head; whether you can achieve this is another question.
  16. http://www.jbjs.org.uk/cgi/content/abstract/76-B/2/210

    There are a number of points that should be borne in mind when we interpret this study, not least that the study employed a specific type of foot orthoses. Kilmartin employed what he described as "modified Root" devices, it is difficult to ascertain exactly how "modified" these were from a strict Root protocol. We do know that similar devices were shown to decrease 1st MTPJ dorsiflexion:


    Although this was by a small amount.

    The point being, that we should extrapolate this data with extreme caution to devices employing other modifications, e.g., plantar fascial groove, reverse Mortons extension, 1st ray cut out, kinetic wedge etc. And to other (adult) populations. As these were not tested.

    On an individual basis, how do we know if the normal natural history of the deformity has been influenced by orthotic intervention? Cessation of progression is easy, but how do we know if we have slowed it down or not?

    Also, N.B. Orthoses aren't the only fruit:

    British Journal of Podiatry November 2004 ; 7 (4): 101-105
    Conservative treatment of juvenile hallux
    valgus - A seven-year prospective study
    Andrew J H Macfarlane, T E Kilmartin

    This study has demonstrated that night splints can, over an average of 3
    years treatment, prevent the deterioration of juvenile hallux valgus and
    subsequent development of associated deformities of the other digits. There
    is clear justification for deferral of surgical reconstruction until
    skeletal maturity when the outcomes of surgery are likely to be more
    predictable. Further, night splint therapy should be considered as a first
    line treatment for hallux valgus.

    As Kevin said:
  17. Furthermore, the dynamic excursion of the axis is significant. I've seen feet that in static stance have a medially deviated STJ axis, but during walking their axis moves through a wide range such that in the latter half of contact period the STJ axis is laterally deviated.
    I guess this is another instance where we need to be cautious of static measures being employed to predict dynamic function. Axial position is probably a good predictor of a number of pathologies, the problems come from only looking at it in static stance.:bash:
  18. efuller

    efuller MVP

    Another cause of lateral ankle instability is sinus tarsi syndrome, which is often seen in the pes pancakus feet with medially deviated STJ axes. Talliard documented that there is decreased peroneal activity with this condition. (peroneal activity will increase pressure in the sinus tarsi.) When these people get on uneven terrain they will have instability due to an increased peroneal reaction time. (I don't have the cite off the top of my head.) The lateral tensile issue is "behavioral" not mechanical. It hurts to use the peroneals so they don't use them, even when they need them more on uneven terrain.

    So, even though there is lateral ankle instability, I would treat the medially deviated STJ axis with a varus heel wedge/ medial heel skive.


    Eric Fuller
  19. I would think in 4D and use a contra-lateral.
  20. Jeff Root

    Jeff Root Well-Known Member

    One potentially huge benefit of orthoses is to improve comfort. People can be asymptomatic yet experience fatigue or "tired feet". I have made orthoses for asymptomatic employees, friends, etc. and have often had them prefer to wear their orthoses because they feel more comfortable with them than without them. This is not to say that comfortable orthoses can't produce symptoms, such a knee pain at a later date, but in general people know what feels good to them and as a rule, well designed orthoses don’t produce symptoms elsewhere. Patient “comfort” is an extremely important from of feedback. While some people can achieve this improvement in the quality of their life with OTC devices, some choose or may require prescription orthoses.

    More importantly, the ultimate goal of medicine is the prevention of disease. If tissue stress (related pain) is your primary criteria for how and what conditions to treat, how could you ever prevent disease? If you use structural and functional criteria, such as one might find with an asymptomatic juvenile flatfoot with a family history (risk factors) for symptomatology, then you have the potential to prevent disease. Obviously far more research is required before we can arrive at the point where we can say with reasonable certainty that we can prevent disease, but this should be the ultimate goal of orthotic intervention.

  21. efuller

    efuller MVP

    The tissue stress approach is both a theory and a prescription writing protocol. Yes, you could call it altering kinetic parameters. (You often increase force in one location to decrease it in another.) The alteration of kinetic parameters, as Kevin stated is based on mechanical modelilng of the structure. So the prescription writing protocol is based upon the modeling which looks at the forces that caused the problem and how to reduce those forces with treatment. (The tissue stress approach includes crutches.) The other underpinning theories just assume that stress is reduced by following the recipe. If you support the deformity, then stress is reduced. If you remove saggital plane blockade then stress is reduced. That logic does not look at how stress is reduced.

    The post I just made about sinus tarsi syndrome is a good example of basing the prescription on observations of the foot rather than having a pathology specific prescription. In sinus tarsi syndrome you attempt to supinate the foot with lateral instability. HAV is another good example of how tissue stress approach is not just a pathology specific orthotic protocol. In HAV high pronation moments increase the tension within the windlass, which will increase what McGlamry called reverse buckling of the 1st MPJ. (See my paper: The windlass mechanism of the foot a model for patholgy. 2000 in JAPMA. Sorry I don't have the exact cite. Not at home computer.) However, there can be more than one source of high pronation moments. The center of pressure of ground reaction force can be far lateral to the STJ axis causing a high pronation moment. For these feet, you need to shift the center of pressure more medial to reduce the pronation moment from the ground. Or, there can be a high pronation moment from muscular activity. There are some feet with laterally positioned STJ axes that will have constant activity of the peroneal muscles. For these feet, you need to shift the center of pressure more laterally to increase the pronation moment from the ground.

    As an interesting aside, I was looking at a prescription form from a lab that uses pathology specific prescription and notice that they had a check box for HAV caused by forefoot valgus and a check box for HAV caused by an everted calcaneus. Rigid forefoot valgus = laterally positioned STJ axis and Everted calcaneus = medially deviated STJ axis? Probably. Actually, very likely, as the everted calcaneus device had a medial heel skive and the forefoot valgus did not.

    The underpinning theories have to explain the success and failures. There are going to be times when different theories come up with the same treatment. However, there is still a leap in logic between, the deformity is supported and why the HAV feels better.


    Eric Fuller
  22. If only it was as simple as that!:rolleyes: Looks like I wasted my time on my PhD if hallux valgus is caused by either: "forefoot valgus" or, "everted calcaneus". Problem solved then, tis one or t'other. I think not....
  23. Atlas

    Atlas Well-Known Member

    That doesn't gel at all in my mind Eric. That is the 2nd last thing you would do for lateral ankle instability. The last thing might be considering the patient's request for amputation.

    That podiatric over-diagnosis of "sinus tarsi syndrome" is the biggest red-herring in our profession and is confusing this region. You're treatment would be spot on if the ankle incorporated an impingement laterally; but not lateral ankle instability whose nemesis is rear-foot inversion (motion) and/or supination moments (forces) and/or...

    (Note there are rare cases where a lateral instability will coexist with an impingement)

    Physiotherapist (Masters) & Podiatrist
  24. Atlas

    Atlas Well-Known Member

    I agree Kevin, and that is a great summation of underlying causes for lateral ankle instability.

    So in view of your comment that STJ axis location theory can work hand-in-hand with tissue stress model...what do we do for this patient? (with a medially deviated STJ etc....who has lateral ankle instability)

    On one hand we want to respect the pathology of one cardinal issue (instability); yet on the other, we want to reduce the pathomechanics (normalise biomechanics) that are likely to result in other minor pathology. The question is how do we do it?

    Physiotherapist (Masters) & Podiatrist
  25. Ron:

    Good questions.

    The Tissue Stress Theory relies on the concept that we must be able to model the foot and lower extremity to determine what type of stresses (i.e. compression, tension, and/or shearing stress) are most likely acting on an injured structure so that we can design a therapeutic program that will most effectively reduce that stress to unpathologic levels, without causing new injury or pathology. Therefore, we must have a good model of foot function, such as the STJ Axis Location/Rotational Equilibrium (SALRE) Theory, that effectively describes the internal and external forces that contribute to pathologies caused by excessive STJ pronation and/or supination moments in order to allow the clinician to achieve optimum clinical efficiency using the Tissue Stress Theory.

    These same concepts of rotational equilibrium and joint moments of the foot that I have been writing and lecturing about for the past two decades (Kirby KA: Rotational equilibrium across the subtalar joint axis. JAPMA, 79: 1-14, 1989) can also be applied to any joint of the foot and lower extremity to better understand the external and internal forces affecting that joint. Understanding each joint of the foot and/or lower extremity through this type of modeling approach greatly aids the clinician using Tissue Stress Theory in the treatment of various joints of the foot and/or lower extremity.

    In your example above of a foot with a medially deviated STJ axis and chronic lateral ankle instability, I would need to know what the underlying etiology of the chronic lateral ankle instability is in order to know how to most effectively treat the pathology. As Simon and Eric have pointed about, one can not always observe the static STJ axis spatial location in relaxed bipedal stance since the STJ axis can swing widely from lateral to medial, especially during the contact phase of gait. The most likely cause of having a chronic ankle sprainer in a foot with a medially deviated STJ axis that I have seen is an increased range of inversion range of motion at the end of supination of the STJ/ankle complex caused by previous inversion ankle injury and partial/complete rupture of the anterior talo-fibular and/or calcaneofibular ligaments combined with peroneal muscle weakness.

    In this case, I would advise a peroneal strengthening program, a foot orthosis with a slight valgus forefoot wedge and a lace up/Velcro strap ankle brace (or high top shoe/boot) when performing sports activities or walking over uneven surfaces. The peroneal strengthening program would increase the STJ eversion moment generating capacity of the individual during unexpected inversion accelerations of the STJ, the slight valgus forefoot wedge would move the center of pressure more laterally during late midstance to decrease the STJ supination moments during late midstance, and the ankle brace or high top shoe/boot would provide increased STJ pronation moment to the foot/ankle during unexpected inversion accelerations of the STJ to decrease the angular supination acceleration of the STJ. In other words, the clinician using tissue stress theory should be able to deduce, using modeling techniques, how each therapeutic modality most likely functions in order to produce the best therapeutic results for their patient.
  26. pod29

    pod29 Active Member

    Hi Ron

    I think this scenario fits very well with a tissue stress approach to prescribing foot orthoses. On one side of the see-saw (teeter-totter) you have a medially deviated STJ axis with high supination resistance. On the opposing side is chronic lateral ankle instability. An appropriate foot orthoses will find a balance of reducing the pronation moment about the STJ axis without applying too much supination moment that it compromises lateral ankle stability. A rigid shell that is well balanced with lateral midfoot support and possibly forefoot valgus extensions should actually provide increased stiffness to the midfoot and possibly help to stabilise the foot into proplusion.

    We work mainly with footballers(soccer) here and this is a scenario that we see and manage quite commonly. It's all about getting the balance:morning:
  27. Jeff Root

    Jeff Root Well-Known Member


    Does this patient have a significant plantarflexed 1st met (ie 1st ray) and an everted forefoot to rearfoot relationship (ie ff valgus) when you examine the foot non-weigthbearing with the mtj fully pronated and the STJ in the neutral position?

  28. David Smith

    David Smith Well-Known Member

    Ron, Eric and all

    Regarding lateral ankle instability with a medially rotated STJ axis.

    I had this notion in my head that I thought was from something Kevin K had written some time ago about this question.

    This being, that where the foot tends to pronate and may also have a medial STJ axis deviation there may still be a lateral instability when the 1st ray is plantarflexed and non compliant to GRF or there is a genu valgum the causes the medial foot to strike early. In each case the 1st ray will be dorsiflexed early in stance phase. This will inhibit windlass action and result in FncHL, at the same time the peroneous longus will be under a high strain. Due to Saggital plane pertubation at this time, at heel lift the CoP progression may tend to move laterally in an attempt to avoid reduction of CoM velocity and the GRF on the 1st MPJ is reduced rapidly.

    In this time while the PL takes up the slack it does not have the full ability to apply pronating forces that resist inversion of the foot. Where the CoP is tending to move laterally on the plantar foot one might imagine that this would apply pronation moments about the STJ but since the heel is lifting but the stance is still in the braking phase the horizontal GRF will tend to push at an angle approximating 90dgs to the STJ, because it is internally rotated. If the STJ were not internally rotated the horizontal braking force would have a much reduce moment arm due to the due to the trigonometrical effect of the reduce and acute angle of incedence. (EG 300N * 30mm = 12 Nm @90dgs but @20dgs => 12sin20 = 4.08Nm)

    The braking force is decreasing as stance progresses but the lever arm available for the GRF acting on the STJ axis is becoming substantially longer as the heel lifts and so the STJ becomes laterally unstable as supination moments increase.

    Does this sound feasible? Did Kevin K say something like this (Saggital plane pertubation (block) not withstanding of course :))?

    Reards Dave
  29. CraigT

    CraigT Well-Known Member


    I will say that I have seen many patients over the years who have markedly pronated feet- medially deviated STJ axes etc- who report a tendancy to roll their ankle for no apparent reason. This is rarely the reason they are seeking treatment, however they often report that this stops following the use of orthoses. These are often aggressive inverted or skived devices (accounting for the STJ deviation).
    However a key feature will always be good lateral column support as Luke mentioned above- (he is a wise man). The Fettig, Feehery (sp?) and Denton mods do this.

    I have a couple of theories as to why this may be.
    One may be the improved stiffness of the lateral column gives the peroneals more mechanical advantage. This stiffness is from the shell of the device, but also from the improve function of the foot.
    Another thought is that in a maximally pronated foot, the peroneal muscles are at their shortest length. In this position they are not at their strongest, and any stretch reflex is likely to be delayed. If the foot is suddenly inverted, the peroneal response may be delayed and weaker.
    The controlled inversion/ supination moment of the orthosis may provide a type of preloading?
    Just theorising out a loud...
  30. Jeff Root

    Jeff Root Well-Known Member


    I would also recommend checking the open chain ROM of the STJ. If the patient's heel remains inverted when the STJ reaches its fully pronated position, then at heel strike grf can induce an inversion or supination moment, which in conjunction with an everted ff to rf relationship, can produce significant lateral ankle instability.

  31. Dave:

    Even though I don't exactly follow all you said above, one important point that your posting made me think of is that, during late midstance, the effect of the tensile force from the Achilles tendon on the production of subtalar joint (STJ) supination moment is very significant. Regardless of whether the posterior surface of the heel is "inverted", "vertical" or "everted", the position of the posterior exit point of the STJ axis relative to the line of action of the Achilles tendon will significantly affect the STJ supination moments, and significantly affect the tendency of a foot with an otherwise medially deviated STJ axis, to possibly oversupinate and cause an inversion ankle sprain.

    It is possible, and not uncommon, to have the STJ axis be medially positioned in the forefoot and also be normal to slightly laterally positioned in the rearfoot. In other words, the STJ axis has a larger degree of angulation relative to the sagittal plane than normal. This STJ axis spatial location will allow the gastrocnemius-soleus-Achilles tendon complex to still have a very significant STJ supination moment effect, even though the STJ axis is medially positioned anteriorly. This peculiar spatial location of the STJ axis could cause, during late midstance and propulsion, STJ supination instability to occur.

    'Tis a complex thing, this foot we work on......requiring a lifetime of thought, research and work to just understand a fraction of it's important biomechanics.
  32. Atlas

    Atlas Well-Known Member

    You've probably had more experience in mucking around with FF to RF relationships. I thought that most feet I see have an everted FF-RF relationship when I examine them with the MTJ fully pronated and the STJ in neutral....

    When I first learnt this stuff years ago, I got excited. But in reality, how relevant is it if its not rigid; and symptoms are not in the forefoot?

    Physiotherapist (Masters) & Podiatrist
  33. efuller

    efuller MVP

    Did you read my rationale. One cause of ankle instability is an increased peroneal reaction time. One cause of increased peroneal reaction time is sinus tarsi syndrome which is caused by Maximal pronation of the STJ.

    I don't understand what you mean by sinus tarsi syndrome being a red hearing. Are you saying it does not exist?


    Eric Fuller
  34. Atlas

    Atlas Well-Known Member

    Eric, this course of action would be fine if we are discussing lateral ankle impingement....not lateral ankle instability.

    I read your rationale, but the 2nd last thing I would do with any lateral ankle instability is invert the rearfoot (motion) and/or up the ante on supinatory (sic sorry KK, but I like this term) forces.

    No. I am saying it is over-diagnosed, over-targeted, and overrated by the podiatry profession. When we, as a profession, begin to understand ankles, lunges, impingements etc., 'sinus tarsi syndrome' will finally be put in the nth-order issue draw of priorities....where it belongs.

    Physiotherapist (Masters) & Podiatrist
  35. sneakyphil

    sneakyphil Welcome New Poster

    i like these ideas. i know that from my own personal experiance, i'm much much more likely to sprain my ankle when i'm NOT wearing my RF inverting DC wedge orthoses. i'd been thinking that it might be related to having too much "slack" in the perroneal tendons because of my severly pronated, medially deviated STJ axis, abducted gait. and this lack of preloading of these tendons could make their reaction to sudden ankle inversion delayed and innefficient.

    anecdotal, but interesting.

    Phil Marshman
  36. Jeff Root

    Jeff Root Well-Known Member

    If the patient has a limited range of calcaneal eversion (ie heel can't reach vertical)and an everted ff to rf relationship, it can contribute to inversion ankle sprains. If the patient has a plantarflexed 1st ray or an everted ff, then grf will tend to create a 1st ray dorsiflexion moment. If the 1st ray can't dorsiflex enough to bring the lateral ff to the ground, then the heel inverts. This retrograde force contributes to lateral ankle instability. This is another example of why we need to look at both structure and function.

    My 14 year old son has this condition. He plays soccer (football) and baseball, and formerly played basketball. He never wore orthoses until about two years ago when he began to sprain his ankle. We first treated it with a soft ankle brace but he continued to have sprains. I put him in orthoses that supported his everted ff position to reduce the retrograde inversion of the rearfoot. He uses his orthoses for baseball and but we still have him wear his ankle brace and orthoses for soccer because of the greater potential for ankle injury.

  37. Jeff Root

    Jeff Root Well-Known Member


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