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Biomechanical Explanation/Advice needed

Discussion in 'Biomechanics, Sports and Foot orthoses' started by footphysio, Aug 10, 2008.

  1. Adrian:

    For the younger podiatrist, possibly a little history on this subject may help give a better perspective.

    I started performing the subtalar joint (STJ) axis location technique on podiatry students and patients at the end of 1984, when I was 27 years old, during my Biomechanics Fellowship (July 1984-June 1985) at the California College of Podiatric Medicine (CCPM) in San Francisco. Within 1-2 months of using and developing the technique, I started to see a strong correlation between the patient's STJ axis location and their symptoms. Patients with pronation-related pathologies had more medially deviated STJ axes and patients with supination-related pathologies had more laterally deviated STJ axes.

    These observations made me excited that I may have come across something very significant in regards to the function of the foot and lower extremity that had not been previously taught to me or described before within the medical literature. In addition, my observations, along with my consideration of the mechanical significance of STJ axis location on these observations, led me to write my first paper on the subject and submit it to the Journal of the American Podiatric Medical Association (JAPMA) in the spring of 1986 (Kirby KA: Methods for determination of positional variations in the subtalar joint axis. JAPMA, 77: 228-234, 1987).

    Even though there was a somewhat cool reception to this paper from all my podiatric colleagues and from all of my former biomechanics professors at CCPM, I strongly felt that I was onto something very important in regards to foot function. Upon further consideration of the effects of STJ moments on the motions of the STJ during weightbearing activities, I started to realize that in order to develop an improved theory of foot function, using STJ axis location as the mechanical basis for that theory, it was very important that I would need to give special consideration to the maximally pronated STJ position as a unique rotational position of the STJ. I began to realize in late 1986, soon after I submitted my first paper on STJ axis location, that even though it made sense that increased STJ pronation moments would cause STJ pronation motion and increased STJ supination moments would cause STJ supination motion, the maximally pronated position of the STJ created a dilemma for me to explain how the STJ would react to an alteration in STJ moments while in this rotational position.

    It finally dawned on me in late 1986 that I would need to use the physics concept of rotational equilibrium to explain why the STJ would not pronate more when additional STJ pronation moments were added to the foot and why the STJ would not necessarily always supinate when additional STJ supination moments were added to the foot while the foot rested in the STJ maximally pronated position. I also realized at this time that the observation that some feet were difficult to supinate with foot orthoses while some were easy to supinate with foot orthoses and that the common clinical condition of sinus tarsi syndrome could also be explained by the concept of rotational equilibrium across the STJ. In addition, I began to understand at this time that just because a foot was in the maximally pronated STJ position, that this rotational position of the STJ did not matter near as much to how the foot would respond to a supination force acting on it as did the STJ axis spatial location. These intellectual landmarks for me led me to submit to JAPMA my paper on STJ rotational equilibrium in May 1988 (Kirby KA: Rotational equilibrium across the subtalar joint axis. JAPMA, 79: 1-14, January 1989).

    Also around this time, in 1988, I was beginning to use the supination resistance test to estimate how much force the posterior tibial muscle (and supination moment) may need to have to produce STJ supination motion in feet with various STJ spatial locations. I first described the supination resistance test in a book chapter I submitted along with Don Green, DPM, in October 1990, on conservative treatment of pediatric flatfoot deformity (Kirby KA, Green DR: Evaluation and Nonoperative Management of Pes Valgus, pp. 295-327, in DeValentine, S.(ed), Foot and Ankle Disorders in Children. Churchill-Livingstone, New York, 1992).

    The reason I am taking the time to describe these bits of history regarding my thought process and events that led me to eventually write and have these papers published on STJ axis location, rotational equilibrium and the supination resistance test is to allow you to see the mental struggle I had with these new concepts from 20 years ago. If you read these papers sequentially, then you will see that I was offering a mechanically coherent explanation for experimental observations that occurred 15 years after my papers were published where it was noted that the kinetics of the STJ are changed more by custom foot orthoses than are the kinematics of the STJ (Williams DS, McClay-Davis I, Baitch SP: Effect of inverted orthoses on lower extremity mechanics in runners. Med. Sci. Sports Exerc. 35:2060-2068, 2003). These experimental observations in runners with different orthosis designs make complete sense if one considers the models I drew for my 1989 rotational equilibrium paper which show that unless the STJ supination moments from an orthosis can exceed the STJ pronation moments from ground reaction force, and take the patient out of their maximally pronated STJ position, then only the kinetics of the rearfoot will change, not the kinematics.

    I hope this gives a better description of how these ideas developed so you can appreciate the thought processes involved and the timing of how these concepts were first introduced to the podiatry profession during my early podiatric medical career.
     
    Last edited: Aug 24, 2008
  2. CraigT

    CraigT Well-Known Member

    Excellent thread!
    Going back a bit- I am not sure if this was answered...
    I don't know about it being widely accepted, but this was the original formula for level of inversion that Richard Blake proposed.
    I think the understanding and appreciation of the role of kinetics in injury management is a vitally important concept. However do you not think that motion is still an important consideration? Perhaps this is what Adrian was suggesting.
    Looking at the example of Tib Post overload.
    You will most likely have a medially deviated subtalar axis which may prompt you to apply (for example) a medial heel skive- this will decrease the total pronatory force on the tendon which should decrease symptoms.
    However- if you apply enough force that you can in fact stop the foot from driving so far into that pronated position- ie change the kinematics- then you will also be preventing the STJ axis from deviating so medially, which will also decrease the force on the tendon. Would this be a result which is more favourable???
    I describe this to non Pods as a continuam- you have to first do something about the force before you can change the movement... but do not discount the importance of this as if you can change the position, you can also influence the force.

    Craig P- have you a comment on another study from Iren Davis' group? I have not got a full copy yet- it looks interesting... can anyone forward a copy???


    Short- and long-term influences of a custom foot orthotic intervention on lower extremity dynamics.
    MacLean CL, Davis IS, Hamill J
    Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine
    Biomechanics Laboratory, Department of Kinesiology, University of Massachusetts-Amherst, Amherst, Massachusetts, USA. cmaclean@parisorthotics.com
    200807

    18(4):338-43

    Language: eng

    Country: United States

    OBJECTIVE: The objective of the current study was to analyze the influence of a short-term and long-term custom foot orthotic (CFO) intervention on the lower extremity dynamics in a group of female runners with a history of overuse running knee injury. DESIGN: Descriptive laboratory study. SETTING: University of Massachusetts Biomechanics Laboratory, Amherst, MA. PARTICIPANTS: This study included a group of female recreational runners (15 to 40 km per week) who had a history of overuse running knee injury in the 6 months leading up to the study. INTERVENTION: Semi-rigid, custom foot orthoses manufactured from a neutral suspension cast and designed to meet the specific needs of each subject. Subjects wore the custom foot orthoses during all running activities for a period of 6 weeks. MAIN OUTCOME MEASURES: Three-dimensional ankle and knee dynamics were collected while subjects performed over-ground running trials with and without a CFO intervention. Data were collected before and after a 6-week CFO intervention during all running activities. RESULTS: For ankle parameters, short-term intervention led to significant decreases in maximum values for rearfoot eversion angle and velocity, impact peak, and loading rate. Ankle inversion impulse was also significantly decreased during the loading phase. At the knee, maximum knee external rotation moment was significantly increased when subjects wore the custom foot orthoses. CONCLUSIONS: The 6-week intervention led to subjective changes, including a significant decrease in pain. An improvement in symptoms did occur with the 6-week intervention. In addition, dynamic results revealed that custom foot orthoses have an immediate effect on dynamics and that this influence occurs only when orthoses are worn in the footwear. The short-term CFO intervention led to significant decreases in rearfoot kinematics (maximum eversion angle and velocity) but no changes observed in knee kinematics. The kinetic analysis revealed that these subjects exhibited significant decreases in maxima for ankle inversion moment and angular impulse during the loading phase, impact peak, and vertical loading rate with short-term, CFO intervention. At the knee, the CFO condition led to increases in knee external rotation moment maxima and angular impulse.
    PMID: 18614885


    Thoughts??
     
  3. Craig Payne

    Craig Payne Moderator

    Articles:
    8
    I am very familiar with Chris's study. BUT, when they said in the abstract about the significant decreases in rearfoot motion, they are talking about a max eversion of rearfoot of 6.28 degrees without orthotics and 5.2 degrees with them - that 1 degree difference was statistically significant, but what is the biological significance of 1 degree? HOWEVER, if you look at the numbers for the change in kinetics - esp the ankle inversion moment (the 'Holy Grail'), then the magnitude of the changes were huge and had p values down to <0.001 ... sorry I no have the actual values handy. Those reductions in the ankle inversion moments will have huge effects on how hard the post tib muscle has to work.
     
  4. David Smith

    David Smith Well-Known Member

    Eric


    You wrote
    This is the reply I gave to a very similar question of, how can a valgus f/f post reduce pronation? on another site.

    "If the forefoot is valgus then it is possible that the 1st ray will have early ground contact relative to the lesser rays. Therefore there may be early dorsiflexion and large RoM of the 1st ray. This may cause excessive stretching of the plantar fascia which in turn will cause excessive plantarflexion moments of the hallux. This will result in high pressure sub hallux and relatively low pressure sub 1st MPJ. This, according to Dananberg and my research is the precurser for FncHL. Moments due to excessive dorsiflexion stiffness caused by FncHL will tend to slow the velocity of the CoM prior to its optimal position for the Lamda model of gait progression IE, due to the force of gravity, the CoM is still falling backwards . In this case there are several compensation options open to the CNS operating system - one is to allow the foot to pronate (perhaps by toeing out more) and increase RoM thru the saggital plane and decrease the fore foot lever length available to the GRF.
    By adding a valgus post to the fore foot this will change the relative timing of the 1st ray to lesser ray dorsiflexions and take force off the 1st MPJ thus reducing hallux plantarflexion moments and therefore reducing or resolving FncHL and the later compensations. Therefore, in this case, a valgus wedge will reduce pronation."

    Eric, Do you agree with this explanaition?

    Dave Smith :morning:
     
  5. A valgus forefoot wedge does not always decrease pronation. However, the times that it does decrease pronation and increase supination seems to be when it directs the CoP to be more lateral in late midstance so that the central nervous system recognizes that it can activate the gastrocnemius, soleus and posterior tibial muscles more, and for a longer period, in late midstance and propulsion without causing the excessive subtalar joint supination moments that would cause lateral ankle instability during propulsion.
     
  6. efuller

    efuller MVP


    Hi David,

    I agree with Kevin's explanation of why a forefoot valgus wedge would decrease STJ pronation. To add to his explanation, the forefoot valgus wedge increased pronation moment and a more everted STJ position. In this position the center of pressure is more likely to be more lateral to the STJ axis and ground reaction force will have a higher pronation moment and the CNS will not feel the need to add a muscular pronation moment from the peroneal muscles at the same time Achilles tension is simultaneously causing an ankle plnatar flexion moment and a STJ supination moment.

    David, As to your explanation: how does a forefoot valgus wedge affect the progression of the center of mass. You note that the progression of the center of mass is slower with FnHL. Dannanberg attributes this to sagittal plane blockade of motion. If a force from the ground is going to slow progression of the center of mass it should be as far anterior to the center of mass as possible. Physics explanation. There is a force couple created by vertical ground reaction force and the force of gravity acting on the center of mass. When ground reaction force is anterior to the center of mass there will be moment causing an angular acceleration to rotate the body backward. Pratcical examples: The jump stop in basket ball. Running at full speed, you jump and land with your feet ahead of your body and you will slow down.

    The reason that I describe this is that Danenberg has described a delay in calcaneal unweigthting in the presence of functional hallux limitus. This is not consistant with a ground reaction force causing a slowing of the center of mass.

    A different explanation of the delay in calcaneal unweighting is that there is a smaller plantar flexion moment at the ankle because the individual has chosen to have a smaller activation the muscles attached to Achilles tendon. The person chooses this because it will hurt more to try and plantarflex the ankle with a functional hallux limitus than without a FnHL. The smaller ankle plantar flexion moment will lead to less power added to the soon to be swing leg. There will be more power added to the soon to be swing leg from hip flexor muscles and this will slow the center of mass because when the trunk pulls the swing leg forward, the swing leg pulls the trunk backward. That is my explanation of why you see a slower progression of the center of mass with FnHL.

    My original comment about trying to explain why a forefoot valgus wedge decreases pronation was directed at those who believe in the neutral position paradigm. I wanted to see if anyone could explain it within the paradigm.

    Cheers,
    Eric
     
  7. David Wedemeyer

    David Wedemeyer Well-Known Member

    This thread came at a great time for me in my reading and research. I admit it is profoundly challenging to relearn and to think of foot pathology in kinetic terms as discussed in the Tissue Stress Theory and to separate it from purely an almost entirely kinematic, mechanical approach.

    Of course this leaves me with more questions than answers at this point, but I feel that I am beginning to understand the points that Craig, Eric, Kevin and Simon are sharing. If I understand correctly then a large part of the Tissue Stress Theory is based on kinetics or moments and GRF would play a large role in this theory? Also the site of complaint should be addressed as the tissues affected by these moments?

    If that is true then kinematics or motion and the anatomical faults we see that contribute to dysfunction in gait is the result of these kinetic changes and not simply anatomic or postural? In Eric’s example then pronation is not the culprit but the slowing of pronation thus causing stress to the tissues, in this scenario it could be the peroneals and in particular the brevis causing 5th MTP pain for example?

    So in that scenario if we see this person has say a laterally deviated STJ then moving the STJ more medial with a lateral skive would increase pronation ‘moments’ about the STJ axis thus possibly decreasing the workload of the peroneals, aiding them in pronation and decreasing GRF and thus tissue stress?:confused:

    This goes back to Simon’s see-saw example where the fat kids are sitting on the lateral side of the foot (the lateral STJ axis and the peroneals) and the other side of the saw is the force of pronation moments, which is really quite inefficient. The fat kids win and the foot tries very hard to pronate but due to the laterally deviated STJ (fat kids) there is a conflict and this stresses the peroneals? If we change the axis of the STJ more medially it slides those fat kids more medially and we have a greater mechanical advantage, greater GRF and less conflict during pronation (actually an increase in pronation moments), which equals decreased tissue stress on the peroneals?

    We are changing ‘moments’ about the rotational axis of the STJ but wouldn’t that also changes the kinematics although the goal is to focus on the former?

    How far off am I?:eek:

    Writing that just raised several more questions but getting my head around this thread is really a challenge!

    Regards,
     
  8. footphysio

    footphysio Member

    My head literally hurts trying to grasp all this biomechanical information. I am trying to make sense of it all as this way of thinking is relatively new to me.:wacko: All this talk about FncHL, COM and compensations makes me think of a current client I have and several past clients with the same characteristics. The past few replies may help to explain the biomechanics behind their pathologies. May be some of you could help me put this together.

    This fellow I am seeing is extremely fat (Simon opened the flood gates for being completely frank). He presents with distal Achilles pain. He has an out toed gait with a midfoot strike and pushes off through the lateral rays rather than the 1st ray. He has a FncHL, forefoot valgus and medially deviated STJ. My thinking here ( after reading the last few posts) is first of all, ff valgus leads to FncHL by way of Davids Smith's explanation. FncHL leads to decreased forward progression. His centre of his extremely large mass is pushing down on his medialy deviated STJ giving a strong pronation moment. His plantar flexors are now working really hard to plantar flex and supinate, especially since his windlass mechanism will not assist due to the FncHL (hence Achilles pain). In the end he out toes and pushes off through his lateral toes because he cannot go through 1st ray due to pain. He also has really tight gastroc/soleus. I'm not sure how I can tie that in other than it causing the midfoot strike and contributing to the pronation and outtoeing as well as his Achilles pain.

    So, to help this man would a logical first step (other than professional dietary advice) be to use an orthotic ff valgus post?

    BTW, does this type of gait seem to be common with obese people? I may be noticing a trend in my relatively short time in practice.
     
  9. So the tissue under stress is the achilles. What is the function of the achilles and what forces would cause it to be excessively stressed? What would be the best way to reduce said stresses?
     
  10. Craig Payne

    Craig Payne Moderator

    Articles:
    8
    Interesting you should raise this. I was going to start a thread on it at some stage.

    For some time I struggled with the rationale for using foot orthoses in achilles tendonitis. None of the risk factor studies showed xs foot pronation as a risk factor.... etc etc .... BUT, so many claim clinical success with the use of foot orthoses.

    Then I got thinking ... what is the function of the muscles attached to the achilles tendon? If they do not have to work as hard, then the loads through the achilles would be reduced.

    The function of the muscles are:
    1. Provide a plantarflexory moment at the ankle joint
    2. Provide a supinatory moment at the STJ
    (ignore the gastroc effect at the knee for now)

    So if we are to reduce loads in the achilles tendon with a foot orthotic, then we need to reduce those moments....ie incorporate design parameters into the foot orthotic to change those moments.

    A heel raise has been the mainstay of achilles management, but I not so sure it actually reduces the plantarflexory moment (I think Sharon Dixon's study showed that, even thou it was a very small sample size). - a heel raise shortens the distance between origin and insertion, but I just can't see how that would reduce how hard the calf muscles have to contract during gait :confused:

    I can't think of a foot orthotic prescription variable that would reduce the plantarflexion moment.

    A heel raise may reduce the supinatory moment (we showed a ~12% decrease in supination resistance force with a 1cm heel raise)

    Certainly and 'anti pronatory' motion orthotic will reduce the supinatory moment (doesn't actually matter if it changes the motion or not), as long as the moment is reduced --> less load on the achilles as calf muscle do not have to contract so much to provide the supinatory moment at the STJ.

    SO, I now think there is a theoretical rationale for using foot orthoses in achilles tendon problems ... we just need data to back it up. Shannan Munteanu, in the Dept here, has funding for a RCT of foot orthoses in achilles tendonitis ..so watch this space.
     
    Last edited: Aug 28, 2008
  11. efuller

    efuller MVP

    Hi David,

    Yes, the site of complaint needs to be addressed. Things break when placed under too much stress. You have to reduce the stress on the broken structure to allow healing.

    David, Have you read Kevin's Rotational equilibrium paper? The diagrams are very helpful in understanding how muscle forces relate to tissue stress. I don't see peroneus brevis causing 5th met head pain. If there is range of motion of the STJ available then the peroneus brevis can create a pronation moment that will evert the forefoot and reduce ground reaction force on the 5th met head. If range of motion of the STJ is not available then peroneal tension will not evert the foot and the 5th met head will have high forces, regardless of whether there is tension in the peroneal tendon.

    A person with an extremely deviated STJ axis will likely have the center of pressure of ground reaction force (average point of force) medial to the STJ axis. This will cause a supination moment from ground reaction force. To prevent supination, and keep the forefoot flat on the ground, the peroneals will have to contract to create a pronation moment that is greater than the supination moment from ground reaction force. This can lead to high stress in the peroneal muscle and tendon.

    So, a lateral skive, or better, a forefoot valgus wedge (The forefoot wedge has a longer lever arm on the STJ axis than the heel cupl of the orthosis, but both could be used) would evert the STJ and this eversion will cause a more lateral projection of the STJ axis onto the transverese plane. So, yes this decreases the supination moment from the ground and hence decreases stress in the peroneal tendons when compared to the situation without the wedges.

    It doesn't really change the magnitude of ground reaction force. It changes the location of the center of pressure relative to the STJ axis which changes the moment from ground reaction force. See my JAPMA paper on Center of pressure.


    David, I think you are close. I'll give you an example with numbers that may help. The center of pressure is 1 cm lateral to the STJ axis and we have a 700 N person standing. This causes a 700Ncm pronation moment from ground reaction force. Rotational equilibrium tells us that when there is no acceleration the net moment must equal zero. So, there is a supination moment from some source, or sources that totals 700Ncm to give a net moment of zero. One possible source of supination moment is the floor of the sinus tarsi. So, if we place a wedge under the foot and shift the center of pressure to a point that is 0.5 cm lateral to the STJ axis and the pronation moment from the ground is not 350 Ncm. The stress will have changed without the position changing.

    Now take that same foot and instead of a wedge start increasing supination moment from the posterior tibial tendon. The pronation moment from the ground is 700Ncm. If the posterior tibial tendon and the floor of the sinus tarsi are the only sources of supination moment: slowly increase tension in the posterior tibial tendon. When there is 100Ncm supination moment from the tendon there will have to be 600 Ncm moment from the floor of the sinus tarsi. The position of the joint will not have changed.

    Now increase the tension in the tendon so that there is a 720 Ncm this creates a net supination moment of 20 Ncm at the STJ. The STJ will supinate. As the STJ supinates there is a lateral shift of the center of pressure that will increase the pronation moment from the ground. When the foot stops moving the center of pressure will have dmove far enough so that the pronation equals the supination moment. So motion will have occured and at the final equilibrium postion there will be zero force in the floor of the sinus tarsi.

    As tendon tension increased force in the sinus tarsi decreased up until the point where motion occured and contact in the sinus tarsi was lost. So just before motion occured the force in the floor of the sinus tarsi was approaching zero because most of the supination moment was coming from the tendon. So, yes when we see motion of the STJ we know the force in the floor of the sinus tarsi is zero. But when we see contraction of the tendon when the STJ is still at end of range of motion we don't see any external signs of reduction of force in the sinus tarsi.

    I hope this helps.

    Eric
     
  12. David Smith

    David Smith Well-Known Member

    Eric

    You wrote
    I completely agree with your explaination, however I see this as a compensation to the tendency for the CoM progression to slow down early in the gait cycle. The compensation you describe allows progression of the CoM.

    I would say that it is also possible to have delayed heel lift and increase in moments about the ankle (where increase in moments means an increase from one side of the equation or the other, in this case I will choose applied GRF times lever arm of the foot to the ankle joint, the opposing moments come from the force of the decelerating CoM times lever arm to the ankle).

    When the hallux has increased applied GRF this will increase the lever arm to the ankle joint and so increase dorsiflexion moments. This can only happen because there are equal and opposite moments acting accross the talo crural joint applied by the achilles tendon and the inertial force of the deceleration CoM. If the heel remains on the ground longer (delayed calcaneal unweighting) then tension will rise in the achilles tendon and at this point there will be relatively increased moments about the ankle joint. This of course will result in increased Achilles tendon strain (it stretches so this enables the heel to remain on the ground) and also increased strain in the opposing structures. Increased strain may result in pathology and or pain and at some point the person/CNS will decide to compensate in some way to reduce these forces, perhaps in the way you describe but not limited to that.

    Cheers Dave
     
  13. For those not familiar with the study Craig refers to its here:
    http://www.uni-duisburg-essen.de/~qpd800/FWISB/Manuscr/Dixon05.pdf

    The peak achilles force decreased in their sample but not significantly. However, the rate of loading was significantly decreased by the heel lifts- the authors suggest that rate of loading may be clinically important. Due to the visco-elastic nature of the achilles, the heel lift should result in a more compliant (less stiff) achilles.

    This study also found similar results but without the timing differences:
    http://cat.inist.fr/?aModele=afficheN&cpsidt=3484945
    "The results showed that, typically, a small initial dorsiflexion moment took place changing into a larger plantarflexion moment before 20% of stance phase. The magnitude and time of occurrence of the initial dorsiflexion moment were significantly affected by heel height changes, but the maximum plantarflexion moment and its time of occurrence were not significantly affected. The results did not support the speculation that a heel lift generally decreases the Achilles tendon loading during running. However, single subject analyses indicated that for two subjects the plantarflexion moments decreased with increasing heel height"

    This is another study of interest here:
    http://linkinghub.elsevier.com/retrieve/pii/S0966636202001960
     
  14. efuller

    efuller MVP

    Dave, I agree that your analysis is possible. However, if that were the correct explanation you would see the center of pressure far anterior to the ankle joint. The FnHL folks describe a delay in calcaneal unweighting (The center of pressure is staying posterior.) The difference between "unweighting" and loss of contact is important. If it were ankle plantar flexion moments slowing gait then you should see an anterior shift in center of pressure.

    Cheers

    Eric
     
  15. Eric and Colleagues:

    I like Eric's argument here. I might add that the functional hallux limitus (FnHL) does not need to "hurt" in order for the central nervous system (CNS) of the individual with FnHL to alter the timing of the contractile activity of their lower extremity musculature. I believe that the CNS is be able to recognize that increased gastrocnemius-soleus complex (GSC) firing during propulsion will be an inefficient mechanism for progressing the center of mass (CoM) forward when FnHL exists. Therefore, the CNS reduces the GSC contractile activity in late midstance and propulsion since it recognizes that using increased GSC contractile activity would be an inefficient mechanism of progressing the CoM forward. Due to the decreased GSC contractile activity, there will naturally be a delay in calcaneal unweighting. I just read a paper that supports the idea of ankle push-off and hip pull exchange that supports Eric's contention of this mechanism. I believe this is derived from David Winter's data. When I find the paper in my stack of journals that I just got, I'll discuss it further.
     
  16. Dananberg

    Dananberg Active Member

    Hi,

    Thought I would join in for a while.

    I would like to address the 1st patient, as this may be the easiest to describe. In subjects who wear out the lateral side of their shoes....using any type of medial posting, skiving or other inverting orthotic Rx is doomed to failure. She is clearly walking on the lateral side of her foot...what causes this?

    Subjects such as this are most often in equinus. When this exists, the peroneal musculature is inhibited, while the antagonist posterior tibial exhibits normal strength. The inhibited peroneals cause two phenomena.

    1. They are unable to maintain the 1st ray in a plantarflexed, everted position, and thus promote a functional hallux limitus
    2. They are further unable to counterbalance the inversion created by the normal facilitated posterior tibial group, and thus the foot appears with a valgus foot type as form follows function.
    3. The PFS is most often related to this process, as the lack of ankle joint dorsiflexion is accommodated by a flexion of the knee in the mid-single support phase of stance. This significantly overloads the patellar and eventually produces the knee pain symptoms.
    4. The longer they perform this flexed knee gait, the greater the likelihood that the popliteus (which supports the knee in the extended position, and resists external rotation) also become inhibited.

    Treatment involves manipulating the ankle and proximal tibia. The orthotic device should be 0 degrees in the RF, and from the sounds of your description, the L side appears shorter (ie, less pronation, more inversion) and may require a small heel lift. Watch for which arm swings more when she walks....it is a very helpful sign and is most often on the shorter of the two limbs. The device will also require a small amount of valgus post on the forefoot, and cutouts for the 1st ray. The last and very important addition is that the device MUST have some type of FF extension either to the sulcus or end of the toes. This is due to the tendency to propulse from the lateral side of the foot. They will tend to move the distal orthotic medially in the shoe, and the FF extension prevents this from occuring.


    Hope this helps.

    Howard
     
  17. Ground reaction force (GRF) is the primary external loading force on the body that creates the internal forces and moments on the structural components of the foot and lower extremity that, in turn, cause the myriad mechanically-based injuries we see on a daily basis in the human foot and lower extremity.

    The specific tissue which is injured must be identified in order for the clinician to direct the treatment toward reducing the pathological stresses on that tissue that is causing or perpetuating that injury in the patient.

    Anatomical variation will definitely cause a change in moments and forces both externally and internally within the foot and lower extremity. However, measurement of externally apparent structural deformities does not always correlate to function and/or pathology. Therefore, using a modelling approach that uses our knowledge of foot and lower extremity anatomy, our knowledge of the types of forces and stresses each specific anatomical structure most commonly receives during weightbearing activities and our knowledge of how we can reduce those forces and stresses within the body of the patient is the key to the tissue stress theory.

    The increase in ground reaction force (GRF) lateral to the STJ axis will not necessarily cause a medial shift in the STJ axis. However, it will definitely cause an increase in external STJ pronation moments which may, or may, not cause STJ pronation and a medial shift in the STJ axis, depending on whether there are any counterbalancing STJ supination moments preventing the STJ pronation.

    David, you are getting the basic concepts. It would be helpful to reread my papers on the subject again when you get a chance since I think they will make more sense now that you are becoming more aware of the concepts.

    Kirby KA: Methods for determination of positional variations in the subtalar joint axis. JAPMA, 77: 228-234, 1987.

    Kirby KA: Rotational equilibrium across the subtalar joint axis. JAPMA, 79: 1-14, 1989.

    Kirby KA, Green DR: Evaluation and Nonoperative Management of Pes Valgus, pp. 295-327, in DeValentine, S.(ed), Foot and Ankle Disorders in Children. Churchill-Livingstone, New York, 1992.

    Kirby KA: The medial heel skive technique: improving pronation control in foot orthoses. JAPMA, 82: 177-188, 1992.

    Kirby KA: Subtalar joint axis location and rotational equilibrium theory of foot function. JAPMA, 91:465-488, 2001.
     
  18. Dave:

    I agree with Eric's analysis. I don't think that the center of mass (CoM) is necessarily slowed with functional hallux limitus (FnHL) since I believe that the central nervous system (CNS) tries to make the body as efficient as possible and tries to conserve momentum of the CoM over the planted foot. As such, since a FnHL prevents normal hallux dorsiflexion, I believe that with a FnHL the CNS alters the timing and magnitudes of firing pattern for the gastroc-soleus complex and hip joint flexors so that smooth, undecelerated motion of the CoM may occur over the planted foot without hallux dorsiflexion. I don't believe that the FnHL necessarily decelerates the CoM but believe that the CNS directs a decrease in internal ankle joint plantarflexion moment and an increase in internal hip joint flexion moment to compensate for a lack of hallux dorsiflexion during propulsion. I believe this conservation of CoM momentum is the key to understanding the gait compensations of FnHL.
     
  19. David Smith

    David Smith Well-Known Member

    Craig

    You wrote
    This is how I see it, :sinking:
    In the foot where a heel lift is required the range of dorsiflexion motion is at its maximum as the leg approaches vertical in mid stance. The muscle can extend no more and the tendon starts to tension. At the point where internal tension is too high some kind of compensation will take place to reduce internal stress and strain. In diagram A) (only considered the relevant forces for simplicity) the example 1) has increased tension in the ach tendon, which causes or is caused by anterior progression of the plantar CoF and a corresponding slowing of the CoM progression. In example 2) the tendon can reach the same point in gait with less tension, therefore the CoM is decelerated less (0.9m/s^2 - V's - 1.0M/s^2) .
    In the second diagram the heel lift allows the foot to achieve the same relative dorsiflexion RoM but allows the CoM to progress forward so that its line of action is forward of the ankle. Whereas the diagram without heel lift (top) requires the CoM to move another 5dgs or more anterior and in its present position gravity induces moments that resist saggital Plane progression of the CoM over the ankle fulcrum. The Ach tendon is in the same state of tension in both diagrams, however to achieve the desired forward progression the top diagram foot must make some compensation to allow this. This may be extra pronation, as you have pointed out the GSC thru the Ach tendon must exert more force to recover to supination from a more pronated position. So even with a compensatory action the ach tendoon is still under more strain without a heel lift than with it.
    So while it intuitively appears that the shortening of insertion to origin is the reason for reduced tension, it may actually be more that the change in CoM position relative to the foot fulcrum is the key. Does this seem to make sense to you?

    [​IMG]


    [​IMG]


    Cheers Dave Smith
     
  20. Simon and Craig:

    I don't see how heel lifts don't alter the tension within the Achilles tendon. I have seen heel lifts immediately reduce the pain in hundreds of patients with Achilles tendinopathy and retrocalcaneal bursitis and immediately reduce the pain in children with Sever's disease. If the heel lifts are not reducing the tensile force within the Achilles tendon, then how do you explain the near instantaneous reduction in pain in these patients when they first start walking with heel lifts?
     
  21. Dave:

    Good to see your diagrams. I did a nearly identical drawing about 20 years ago to explain how heel lifts reduced Achilles tendon tensile forces.

    I believe that heel lifts probably have a much greater effect in reducing Achilles tendon tension on those patients that have a relatively shortened gastrocnemius-soleus complex (GSC) than in those patients that have the more normal 10 degrees of ankle joint dorsiflexion. The central nervous system (CNS) is unlikely to compensate for a short GSC by inefficiently attempting to lengthen the GSC with increased out-of-phase muscular activiation of the ankle joint dorsiflexors (e.g. anterior tibial muscle) during late midstance phase. However, the CNS may easily compensate for a normal to long GSC complex that has a heel lift added by increasing the contractile activity of the GSC to the exact level of ankle joint plantarflexion moment that is required for smooth progression of the center of mass over the planted foot.
     
  22. Kevin,
    Don't shoot the messenger. I agree. I have also successfully employed heel lifts in association with other prescription variables in the treatment of the conditions you list.

    I would also tend to agree that the research really needs to look at symptomatic subjects.

    The paper at the last link I included in my previous post appears to address the issue of variation in dorsiflexion "flexibility" at the ankle and this too demonstrated no differences in ankle joint moments or kinematics during walking between those with high "flexibility" and low "flexibility" (I'm not sure how they determined "flexibility" as I don't have the full text, however I assume they are measuring range of motion or joint stiffness). From the information in the abstract these results appear to challenge the ideas presented by Dave and previously by yourself, it also challenges my own prior learning and experiences too. Interesting.
     
  23. Dananberg

    Dananberg Active Member

    In my view, the pathologic reality of the CoM's motion and its relationship to FnHL is as follows:

    The CoM is long into its forward motion by the time heel lift has or should occur. The problem is the lack of motion within the foot at the same time as the CoM continues to move forward. This is what creates the "rock and hard place" issue. By either adding a heel lift or producing an orthotic device to manage the functional locking of the 1st MTP joint, the net result is allowing the forward motions to occur simultaneously. When the CoM moves, but the foot doesn't, stress must be present somewhere between the two. Considering this happens 8,000 times/day....it produces a pathological mechanical situation.

    Howard
     
  24. David Smith

    David Smith Well-Known Member

    Kevin

    .

    Ah well you see I've been loooking over the shoulders of giants

    Yes that would make sense

    Agreed, and activating the ant tib would have the sub optimal effect of extending and flattening the MLA at a time when the opposite is required.

    Exactly

    All the best Dave
     
  25. Just doing a little duck hunting.....quack, quack.;)
     
  26. Probably the best way to model the effect of heel lifts on Achilles tendon tension is to consider that the tensile force within the Achilles tendon at the instant of heel off is a combination of both passive mechanical factors and active mechanical factors. Passive mechanical factors include what we commonly measure when we perform a nonweightbearing ankle joint dorsiflexion examination, with no muscular activation, which I call passive ankle joint plantarflexion stiffness. Active mechanical factors include the increase in Achilles tendon tension that arises from central nervous system (CNS) activation of the gastrocnemius-soleus complex (GSC) during heel off, which I call active ankle joint plantarflexion stiffness.

    My hypothesis is that subjects with high passive ankle joint plantarflexion stiffness will show a significant reduction in ankle joint plantarflexion moments during late midstance with the addition of a heel lift whereas those subjects with low passive ankle joint plantarflexion stiffness will show little to no reduction in ankle joint plantarflexion moments with the addition of a heel lift. The passive stiffness within the GSC can not be significantly decreased by the CNS since the passive GSC stiffness is determined by the viscoelastic nature and relative length of the GSC and Achilles tendon. However, the stiffness of the GSC may be significantly increased by CNS activation of the GSC to incrementally increase the GSC stiffness, and therefore also incrementally increase the magnitude of ankle joint plantarflexion moment during late midstance, as the task demands. This hypothesis certainly makes sense from the clinical effects that I have seen on treating Achilles tendon disorders with heel lifts over the years.
     
  27. Craig Payne

    Craig Payne Moderator

    Articles:
    8
    I not disagreeing with the use of heel lifts for severs and achilles tendon probs, its just the simplistic rationale for their use I struggle with.

    Simplistically, if i was to stand and then raise on my toes, x load goes through the achilles tendon; if I added a heel raise (to shorten the distance between origin and insertion) and the raise up on my toes, I can't see how that reduces the load in the achilles tendon ?

    There is no doubt that heel raises help clinically, but by other mechanisms (shock absoprtion; STJ moments; etc)
     
  28. efuller

    efuller MVP

    Hi all,

    We should carefully clarify the condition we are talking about. In static stance with an ankle that dorsiflexes to 0 degrees, I would expect immediate relief with a heel lift in static stance. (A 3.5mm orthotic could act as a heel lift.) Now, in gait, I would not expect much difference in tension if there is equal power output when comparing the lift to not lift condition. Benno Nigg was involved with a study that looked at inverse dynamics and heel lifts and saw no difference in ankle plantar flexion moment with and without the lift.

    Cheers,

    Eric
     
  29. admin

    admin Administrator Staff Member

  30. Second link in my previous post. here again:
    http://cat.inist.fr/?aModele=afficheN&cpsidt=3484945
     
  31. Eric:

    In the hundreds of times I have seen patients with Achilles tendon symptoms, they report that walking with a heel lift makes their symptoms improve. The symptoms don't seem to be that significant with just standing. The symptoms are caused by walking and especially running. If this common clinical observation is not caused by a decrease in Achilles tendon tension, then what do you expect causes this finding? Also, how would I measure in my clinic if there is equal power output when comparing a lift to no lift condition?

    Even though I am aware of the literature, my 25 years of treating these symptoms in countless patients indicates to me that the most likely cause of the reduction of symptoms with a heel lift in patients with Achilles tendon pathology is due to a reduction in Achilles tendon tension. Could the peroneals and deep flexors be more active and the gastrocnemius-soleus be less active with a heel lift?
     
  32. I guess what we are attempting to achieve with the heel lift is to alter the length/ tension relationship of the muscles. The net length/ tension curve being the result of the passive and active components. The current issue of the Journal of Applied Biomechanics includes two articles relating to this. Here is the abstract from the second paper:

    "For a physiologically realistic range of joint motion and therefore range of muscle fiber lengths, only part of the force-length curve can be used in vivo; i.e., the section of the force–length curve that is expressed can vary. The purpose of this study was to determine the expressed section of the force–length relationship of the gastrocnemius for humans. Fourteen male and fourteen female subjects aged 18–27 performed maximal isometric plantar flexions in a Biodex dynamometer. Plantar flexion moments were recorded at five ankle angles: -15°, 0°, 15°, 30°, and 40°, with negative angles defined as dorsiflexion. These measurements were repeated for four randomly ordered knee angles over two testing sessions 4 to 10 days apart. The algorithm of Herzog and ter Keurs (1988a) was used to reconstruct the force–length curves of the biarticular gastrocnemius. Twenty-four subjects operated over the ascending limb, three operated over the descending limb, and one operated over the plateau region. The variation found suggests that large subject groups should be used to determine the extent of normal in vivo variability in this muscle property. The possible source of the variability is discussed in terms of parameters typically used in muscle models."- JAB, 24(3), August 2008, Reconstruction of the Human Gastrocnemius Force–Length Curve in Vivo: Part 2—Experimental Results. Samantha L. Winter, John H. Challis

    The length-tension relationship should be altered through the addition of a heel-lift, shifting the curve to the right of the length (x) axis. i.e. by removing tension in the muscle via the heel-lift it should be similar in effect to a muscle that is functionally long and weak as described by Yanda. So maximal force is then produced at a different point within the joint range of motion, with relative weakness in inner range. The results of the above study suggest that individuals gastroc/ soleus function at varying points within the curve also. The proportional change in muscle groups length/tension that is achieved through lifting the heel may vary among individuals despite the use of identical heel-lifts as per the Dixon and other studies. Indeed, this may go some way to explaining the variable results obtained in the Nigg study. Of note also is that none of the studies thus far have examined the longer term effects of heel-lifts, only immediate response.

    Thinking out-loud, so I hope it makes sense.
     
    Last edited: Aug 29, 2008
  33. Dananberg

    Dananberg Active Member

    Yanda's influential thinking on muscular strength during phases of gait is most important in understanding what the effect of heel lifts actually accomplish.

    Classically, the clinical test of Posterior tibial tendon (PT) rupture or even dysfunction is the single sided heel raise. Considering the normal nature of the Achilles tendon/muscle is this case, the inability to raise onto one's toes when the PT is removed from the equation, raises the question as to what functional structures cause (allows?) heel lift. If we change position of the foot via a heel lift, and this, from a Yanda perspective, changes muscle function in either the PT, peroneals or both, it is that change that relieves the strain on the Achilles tendon and thus decreased symptoms?

    As Simon said....just thinking out loud.

    Howard
     
  34. I started thinking a little outside of the box on this one. We wear shoes with variable heel height differentials, women especially. Basically, the heel of a shoe is the equivalent to the heel lift on the orthoses. So what does the research which has compared walking in low flat shoes with high-heeled shoes conclude about the effects of heel height on ankle plantarflexor moment? Two minute google search and the first hit:
    http://www.japmaonline.org/cgi/content/abstract/93/1/27

    Kinetics of High-Heeled Gait

    Meltem Esenyel, MD*, Katlen Walsh, Judith Gail Walden, MPH* and Andrew Gitter, MD*

    A within-subject comparative study of walking while wearing low-heeled sports shoes versus high-heeled dress shoes was performed to identify and describe changes in lower-extremity joint kinetics associated with wearing high-heeled shoes during level overground walking. A volunteer sample of 15 unimpaired female subjects recruited from the local community underwent quantitative measurement of sagittal and frontal plane lower-extremity joint function, including angular motion, muscular moment, power, and work. When walking in high-heeled shoes, a significant reduction in ankle plantar flexor muscle moment, power, and work occurred during the stance phase, whereas increased work was performed by the hip flexor muscles during the transition from stance to swing. In the frontal plane, increased hip and knee varus moments were present. These differences demonstrate that walking in high-heeled shoes alters lower-extremity joint kinetic function. Reduced effectiveness of the ankle plantar flexors during late stance results in a compensatory enhanced hip flexor "pull-off" that assists in limb advancement during the stance-to-swing transition. Larger muscle moments and increased work occur at the hip and knee, which may predispose long-term wearers of high-heeled shoes to musculoskeletal pain. (J Am Podiatr Med Assoc 93(1): 27-32, 2003)

    This study from Kevin's research colleague Stephen Piazza seems to concur with my musings on length/ tension: http://www.gradsch.psu.edu/diversity/mcnair_jrnl/files/25_henderson.pdf

    "In high heel gait and standing, many muscles located in the lower extremities and
    the back are overly worked due to the plantar flexion of the foot. Muscles are at their
    peak for force generation when they are at resting length. When muscle length increases or decreases beyond its resting length, muscle force production decreases in a bell shaped form. This relationship is seen in high heel wearers. When the heel is raised, as in wearing high-heeled shoes, muscles fibers that innervate the muscles along the leg are shorten. The shortened muscles are now inconsistent with its resting length-tension relation resulting in less force production. Esenyel et al. (2001), found “… the exaggerated plantar flexed position of the ankle joint places the gastro-soleus muscle at a shortened and thus less favorable position on its muscle length-tension curve. Under such conditions, the plantar flexion musculature is in a less advantageous position for power and work generation and consequently less propulsive abilities. (Esenyel et al.,2001)

    And also seems to agree with the out-loud thoughts of Howard and to the idea that it is the supinatory effect of the heel lift that may be significant: read the discussion!

    So the question then becomes, why do we see changes in ankle kinetics and kinematics with high-heeled shoes but not with heel lifts? Is it because the heel lift studies looked at running while the heel height trials have focused on walking?

    Food for thought, I hope.
     
  35. David Smith

    David Smith Well-Known Member

    Kevin and all

    Kevin said that it may only be those subjects who have short GSC that see reduction in achilles tendon tension with the intervention of heel lifts. I think this may be correct and the diagrams below will help explain this.

    I’ve been doing some diagrams, in between customers, to try and get a feel of what is happening in the Achilles- ankle complex in a person with short GSC. I can’t quite seem to get to a conclusion so I thought I would look for your help.

    First can I suggest that the Achilles tendon does not lift the heel off the ground? All the Achilles tendon tension (Att) does is - 1) to accelerate the CoM, to produce useful inertial force (IF) that induce moments at the forefoot / MPJ's (P) and - 2) keep the CoM in the correct position for efficient forward progression. This spatial position varies dependent on the velocity of forward progression required.

    Diagram
    1) Normal stance = line of action (LoA) of force of the mass x gravity (Fmg) is directly thru the ankle joint (A) and the mass (CoM) has no acceleration horizontally (or angular). Therefore no moments about a and equal moments about MPJ’s (P ) and Heel (C). Therefore no tension required in Achilles tendon (Att
    2) To achieve heel off the moments from the Inertial force (IF) of CoM about P, must be greater than the moments from Fmg about P. The horizontal Force vector of Achilles tendon tension (FAtt) accelerates (negatively) the CoM to achieve this. If this is not achieved, because the CoM has zero velocity, then the body (CoM) will fall backwards onto the heel and come to rest.

    3) In static balance the moments about P sum to zero as the LoA of the CoM passes directly thru P and the horizontal accelerations are balanced by Fmg and Att and so moments about (A) (clockwise and anticlockwise) are in static equilibrium. IE effectively (but not actually) the Att is pulling back while gravity is pulling equally forward.

    4) To continue in forward progression the moments about (A) are still in static equilibrium but the moments about P are not, I.E. Fmg and IF (CoM) are producing anticlockwise moments about P and the CoM progresses forward in an arc toward the ground (PCoM). In order to retard this arc velocity toward the ground (PCoM) the Achilles tendon must tension and shorten at a rate that tend to maintain the height of the CoM and only allow horizontal progression. In this case point (A) would project forward (PA) and C would approximate to CoM. This also allows the ground clearance for the contralateral leg to swing thru.

    5) If the Achilles tendon is short and tight (ankle equines) then it should be possible that as the calcaneous approaches zero load in its un- weighting phase then the velocity of the CoM also approaches zero, then it is possible that there is the situation as described in 2) where the CoM causes clockwise moments about P and the heel becomes weighted again.

    Adding a heel lift at this point would enable the CoM, at some angular elevation, to produce anticlockwise moments about P and forward progression continues due to energy added to the CoM from gravity. If the Nigg et al paper is correct in its theory that heel lifts do not reduce ankle moments then it is difficult to see how they do not in subjects with tight GSC and ankle equines. From my reasoning it seem it is only possible for the CoM to progress if a heel lift is added. However if the CoM velocity is reduced to zero and so its kinetic energy reduced to zero, therefore requiring a heel lift toad gravitational energy and progress, this means that more work must have been done per unit time by the Achilles tendon. So therefore a greater magnitude of force must have been applied by the Achilles tendon or the same magnitude of force for a longer time. The Nigg paper indicated moment magnitude and timings where not changed significantly (statistically at least). It may have been useful to see the force impulse data for the same subjects.

    Maybe when the above scenario (of sub optimally slowed CoM) is approached the tendency to pronate to increase ankle RoM or supinate into early heel lift, changes the internal forces in the Achilles tendon and the force generated is not evenely distributed thru the tendon fibres and therefore there is localised increase in stress.

    I think perhaps that, in the Nigg et al study they did not filter the variable of ankle equinus and their subjects where mostly non equines, except for two who did give outlier data showing increased ankle joint moments.

    [​IMG]

    Anyone got any help for me? :bash:

    Cheers Dave
     
  36. efuller

    efuller MVP

    Hi Dave,

    I disagree with your first assumption. It may be true for some conditions, but not all.

    Achilles tendon tension (Att) will create a plantar flexion moment of the foot at the ankle and create a rearward rotation moment of the head about the ankle joint. Whether this will occur is dependent on several things that include the position of the center of mass and the direction of momentum of the center of mass.

    An increase in Att will cause a forward shift in the location of the center of pressure in the static stance individual. An individual can move their center of mass in anticipation of this shift in center of pressure.

    Example 1: the individual keeps their center of mass directly over their center of pressure as it shifts forward. The Att lifts the calcaneus off of the ground and a static equilibrium is achieved with with the heel off of the ground and the center of mass over the center of pressure. Stand on your tip toes and you will adjust for postural sway with increased and decreased pressure on your toes to shift your center of pressure back and forth to keep it under the center of mass.

    Example 2: increase in Att and the individual keeps their center of mass posterior to their center of pressure. The force couple of body weight and center of pressure will cause a backward rotation of the body. You could see this in the side view of Olympic diving quite nicely when the divers would start falling (rotating backwards) before their jump to get the rotation started. The Att will also work directly to cause a rearward rotation moment of the body relative to the foot as well.

    Example 3: increase in Att and the individual keeps their center of mass anterior to the center of pressure. This is what usually happens in most styles of walking. Att increases as the center of mass passes the center of pressure. This will slow center of mass because it will create a rearward moment on the body and shift the center of pressure forward which will decrease the distance of the center of pressure to the center of mass. However, the center of mass will still be anterior to the center of pressure and there will still be a forward rotation of the body. After opposite limb contact the Att force in connection with ankle plantar flexion can add energy to the trailing leg to help initiate swing.

    This got me thinking as to why a heel lift could reduce tension and pain in the Achilles tendon. When looking at people stand on the EMED I noticed that a vast majority stood with center of pressure anterior to their ankle joint. That is there would be constant tension in the tendon even though the person thinks they are relaxed. A heel lift would alter the anterior posterior balance equilibrium position and the person could choose to balance with their center of mass and center of pressure more posterior and this would put less tension in the posterior tibial tendon. That's a fairly simple research project for someone with an EMED. Research question: What is the average percentage of foot length of the location of the center of pressure in static stance. Does it change with a heel lift? Does it change with a heel lift in people with Achilles tendonitis?

    Just some thoughts,

    Eric
     
  37. David Smith

    David Smith Well-Known Member

    I think were both on the same page but the question of how or whether the achilles lifts or applies moments may just be a question of perspective.

    Re reading the Nigg paper, overall there is an decrease of plantarflexion and dorsiflexion moments that correlates linearly with an increase in heel height and the time to max torque does increase similarly, suggesting a moving forward of the centre of pressure applied to the foot or a slowing of the CoM velocity. These are statistically insignificant and only account for a 4% increase in torque and the assumption can be made that this only equals a 4% increase in achilles tension and stress. Which is less than the sd of AT tension intersubject. It seems unlikely that this would be a clinically significant change.
    However 2 of the five subjects (#3 and #5) did have a very significant decrease in ankle moments that would suggest a correlating decrese in AT tension. 2 subjects (#1 and #2) did not have a significant change and one (#4) had more of a change than these two but not as great as the first two. Therefore, as the paper states these anomalies require further investigation and I would suspect that these outlier data were the result of ankle equinus in those subject where the ankle torque decreased with additional heel lift.

    I could not make out from reading the paper if they evaluated the ankle moment in the local axis set or within the global axis set only. (did anyone figure that out?) Certainly they did state that they could not account for frontal plane deviation but did not mention horizonntal plane deviation. If the moments were only expressed interms of the global saggital plane there may have been some room for error here. All these small areas of error and limitation coupled with the low statistical power may have resulted in conclusions that would be counter intuitive and not reasonable.

    It would seem reasonable to me that to get the CoM to the point where the heel lifts and gravity contributes energy to forward motion requires AT tension. If the AT strain is increased to achieve the same position, due to relative reduction of original tendon /muscle length (Lo), then there must be a correlating increase in stress and tension in the final tendon muscle length (L1).

    Either that, or a compensation is made such as short step length or pronation, or knee hyperextension etc etc. Perhaps these compensations alter the characteristics of internal stress distribution in the tendon.

    Cheers Dave
     
  38. Lawrence Bevan

    Lawrence Bevan Active Member

     
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