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Role of the spring ligament

Discussion in 'Biomechanics, Sports and Foot orthoses' started by NewsBot, May 6, 2008.

  1. NewsBot

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    The effects of sectioning the spring ligament on rearfoot stability and posterior tibial tendon efficiency.
    Jennings MM, Christensen JC.
    J Foot Ankle Surg. 2008 May-Jun;47(3):219-24.
     
  2. Admin2

    Admin2 Administrator Staff Member

  3. Adrian Misseri

    Adrian Misseri Well-Known Member

    Interesting idea, makes a whole lot of sence.

    My only quiery is, given the position, strength and size of the spring ligament, versus the function, position and size of posterior tibial tendon, along with the fact that the tendon undergoes a change of difection over what is a relativately avascular area, one would expect the posterior tibial tendon to fail before the spring ligament in a real world setting. Also bear in mind that the spring ligament is supported in its function by the short and long plantar ligaments. Although a strain of the spring ligament is quite possible, a complete rupture akin to the sectioning described above, to the degree to allow the sort of instability suggested above, would be highly unlikely, and would occur with significant damage to long and short plantar ligaments, also with posterior tibial, flexor hallux longus and flexor digitorium longus tendons. In short, any acute injury to cause the spring ligament to rupture should deform the foot quite aggressively.

    Any thoughts? Am I incorrect in believeing this?

    Good news post though :eek:)
     
  4. Mart

    Mart Well-Known Member

    Hi Adrian

    Although the study looked at sectioning which as you suggest is analgagous to a rupture in real life how about the possibility of chronic irreversable ligamentous stretching from mechanical overload. I recall Doug Richie presenting on this idea a couple of years ago with a neat prepared disection demonstrating this effect.

    This being true, would the rational for prolotherapy into these structures with protective bracing not seem a worthwhile appoach before considering surgery?

    cheers


    Martin


    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
  5. kevin miller

    kevin miller Well-Known Member

    I would really love to have the reference. I am doing research in this area. In fact, I would say they are right, but for the wrong. reason. Mart is right on track when he mentioned the stretching or "plastic deformation" that occurs in all voscoelastic materials, including all human tissues. We are used to muscle healing so quickly that we aren't aware of what is going on in the ligaments. If some one can tell me how to upload a picture, I will show you a terribly deformed posterior tib tendon in a cadaver who had relatively normal feet with some evidence of aquired flat foot in life. The long, short, and spring ligament were all stretched, but I threw out the picture because the stretching was not evident in the photo. I have seen this in every cadaver I have studies that had aquired flat foot deformity.

    The result of having these sturctures plastically deformed was calcaneal plantarflexion and all that implies.

    Kevin M.
     
  6. efuller

    efuller Well-Known Member

    Adrian,

    I'd agree with some and disagree some. I would agree in the real wold (the foot is attached to a brain and there is intact sensation) the posterior tibial tendon will tend to be injured before the spring ligament. Pain avoidance can be seen in many situations. If the spring ligament hurts the person is very likely to use their posterior tibial muscle to decrease tension in the tendon. What Hicks showed over 50 years ago, and Kevin has said in his rotational equilibrium paper is that tension in the posterior tibial tendon will shift the force under the foot more laterally. When the force is shifted laterally there will be less force on the medial metatarsals and more force on the lateral metatarsals. This is where I disagree with what you said earlier about the long and short plantar ligaments having the same function as the spring ligament. Yes, they both prevent dorsiflexion of the forefoot on the rearfoot. However, the long and short plantar llgament prevent dorsiflexion of the cuboid on the calcaneus and the spring ligament prevents dorsiflexion of the navicular on the talus. So, tension in the posterior tibial tendon will shift weight on to the lateral metatarsals and place more strain on the thort and long plantar ligaments and decrease tension in the spring ligament.

    Cheers,

    Eric
     
  7. Adrian Misseri

    Adrian Misseri Well-Known Member

    Thanks guys,

    Great to get some feedback. I guess in a clinical setting we tend to get a bit wraped up in tibialis posterior dysfunction because it seems to be the most obvious cause of that severe medial colapse and bulging (patten recognition diagnosis perhaps?), but certainly there are otehr structured whichare at play and are equally important. Thanks again for the viewpoints back. Would also love that reference when you get around to it martin.

    Cheers!
     
  8. kevin miller

    kevin miller Well-Known Member

    Eric, all,

    Respectfully, during high tension moments, then muscle belly of the Post tib is likely to give the supporting power to the intrinsic ligaments. The is no brain action in this as mechanoreceptors do this locally. In the muscle, it would be the spindal fiber, which seeks to have the same tension on the muscle at all times. This is backed up by the golgi tenson body which loops back through the spinal chord to tell the spindals to lossen up the muscle.

    In addition, the muscle itself does not act the way it does in an open kinetic chain setting. In short, when the foot is on the ground, the Post Tib is no longer an adductor and plantar flexor PRIMARILY, it pulls the lateral column towards the medial side. The other actions become secondary.

    As the lateral column is now without its supporting muscle, the long and short plantar lig get stretched first. The CC joint opens up and the calcaneus begins to plantar flex, stretching the spring ligament and putting more tension on the post tib than it can adapt to. Now you can eplain everything in sequnce that happens prior to post tib failure.

    Kevin M
     
  9. Kevin Kirby

    Kevin Kirby Well-Known Member

    Adrian:

    As Eric stated, the short and long plantar ligaments do not do the same thing as the spring ligament complex. The spring ligament complex (SLC) works synergistically with the posterior tibial tendon to cause a plantarflexion and adduction moment on the talo-navicular joint so that either elongation or tearing of either the SLC or posterior tibial tendon will mechanically affect the other structure. We have known for some time that the SLC is a commonly injured structure in posterior tibial dysfunction and likely the partial or complete failure of the SLC is what causes the gross abduction of the forefoot on the rearfoot that is often seen in more advanced cases of posterior tibial dysfunction. The classic paper on the SLC is by Davis et al and is a must read for you that I have also attached below (Davis WH, Sobel M, DiCarlo EF, et al: Gross, histological, microvascular anatomy and biomechanical testing of the spring ligament complex. Foot Ankle Int. 17:95-102, 1996). It is one of my favorite papers on foot ligaments ever published. In addition, I have previously discussed the mechanical importance of the SLC in a previous invited article from 8 years ago (Kirby KA: Conservative treatment of posterior tibial dysfunction. Podiatry Management, 19:73-82, 2000) which I am attaching below.

    Hope this helps.
     
    Last edited: May 8, 2008
  10. efuller

    efuller Well-Known Member

    Kevin, I'm not quite sure what you are saying. You can't be saying that the brain does not alter the tension generated by the muscle belly.

    Kevin, Again I'm not sure what you are saying. I didn't even talk abouk open kinetic chain. Are you disagreeing with what I said about the lateral weight shift.? I agree that the tendon pulls both the medial and lateral column medially. The posterior tibial tendon plantar flexes very little because its attachment is medial and plantar, but more medial.

    The plantar ligaments primarily prevent dorsiflexion of the CC joint (or plantar flexion of the calcaneus relative to the cuboid.) In posterior tibial dysfunction you lose the lateral pull and you get lateral movement of the cuboid relative to the calcaneus to get the classic too many toes sign.

    An intact posterior tibial muscle will cause supination of the STJ and an increase in lateral forefoot weight bearing. With lateral forefoot weight bearing you will have increased strain of the long and short plantar ligaments. So, the postier tibial tendon does not support the cc joint in the dorsal-plantar direction.

    Kevin, in the beginning of the above paragraph, which muscle are you saying supports the CC joint?

    Cheers,

    Eric
     
  11. kevin miller

    kevin miller Well-Known Member

    Hi Eric,

    Let me address your statements in order:

    No, I am not saying that the brain does not have input, but it is at a different level than we are talking about here. At this level, things happen faster than a nerve signal can travel to the brain and back. The only two other nervous system components are the receptors themselves and the spinal chord.

    You never mentioned the open chain, granted. But the muscle action described originally does occur in the open chain. The foot operates in gait in a closed chain setting. Just as what KK said is true in the open chain setting, what I wrote is true in a closed chain setting. Frankly, we should have supsected as much, it makes since evolutionarily to have multiple functions.

    The Post supports the lat column through is midfoot supination function. The p. longus uses the cuboid/ lat column as a lever to pull the med column laterally and the P. brevis pulls the lat column proximal. In their way, all are supposrting muscles.

    Respectfully,
    Kevin M
     
  12. Mart

    Mart Well-Known Member

    This seems like another of these chicken and egg situations which is difficult to resolve other than through logical reasoning. Because there are no established quantitative measures to evaluate ligament functional properties in vivo over period necessary to study this or ways to isolate this from other functional variables such as accumulated stress I can’t see how it could be otherwise.

    My prior comments were simply recalling some seeds of ideas planted several years ago from Doug Richie’s excellent presentation in Toronto if I recall. No references from me but if I get a moment I'll dig through my archived conference pile and see if there are any useful refs from his PowerPoint notes.

    If I understand Kevin M correctly he is suggesting that reflex protective stabilizing contraction of TP is likely to be more frequent and possibly in absence of protective firing in response to chronic pain stemming from cortical response to ligament strain. The importance would then be that in cases of sub clinical (pain free) recruitment of the TP , the spring ligament (and I agree with those who say we should rename this “sling” ligament) would not be protected by normal TP function. If there is mechanical overload sufficient to cause plastic deformation the natural history would lead to a point where a multitude of possible chronic injury could follow . . . . .traumatic synovitis of joints and tendon, muscular fatigue, then the cascade of end events including bone/ joint remodeling etc.

    This secondary point is where TP overload was then more likely to start and the symptoms of TP synovitis and tearing to start to show up clinically and the inability to perform single limb stance heel raises obvious.


    I’d be pleased is someone could explain why this might be implausible. It is an important consideration because if this scenario is true (not sure it could be proved/disproved) then there would be reasonable argument for “prophylaxic “ foot orthoses use which remains a controversial issue.

    cheers

    Martin

    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
  13. kevin miller

    kevin miller Well-Known Member

    Martin,

    Thank you for putting this so succinctly for me. I have been up to my elbows for 3 1/2 years in feet and it is sometimes hard to articulate a point so clearly.

    Again, it will be difficult for me to explain here with no photos or diagrams, but what I have found is going to change the way we think about foot function.... period.

    For instance, we have thought that the plantar fascia supports the foot at mid stance and the changes its role in activation of the windlass. This is not possible because the plantar fascia splits into slips that allows each Met to float freely as you would expect it to do if it must instantaneously adapt to varying surface topographies, which I believe it is meant to do. The foot as we know it has been in existence 7 million years - longer than homo sapiens have been in on the planet.

    So what does support the foot at midstance? Wrong question........the Mets float. The question is: So what does support the midfoot at midstance?

    Pull out your trusty anatomy atlas and look. The Post Tib and P Longus cross over one another and produce a sling effect and and arching effect on the mid foot. This takes care of the transverse arch. The long arch has the ABductor Hallusis, the lat arch, P brevis. Underlying these are the ligaments in question.


    Right about now someone has asked the question: But why would the foot use the two stronger muscles for the transverse arch and the two weaker ones for the long and short arch?

    Because in its normal environment, the foot needs more support in the frontal plane, where it twists with varying topography during the contact phase. The long and short arch also get a bit of support from the two strong muscles by passing through them. But the greatest aid comes from structural support. When the Pl and PT contract, the joints of the midfoot change their angles slightly and become VERY stable. I have a cadaver foot that has no support other than formalin soaked ligaments and a screw in the CC joint. I can't collapse it with my hands.

    It does seem like a chicken and egg situation because it is. This arrangement of structures evolved together. Where does the egg break? When we put the foot in a shoe and make it operate in essential one or a few degrees of its operable ROM. The shoe acts like a cast, weakening the muscle relatively and the narrow ROM produces a stress reaction.....soft tissues first, but certainly the bones in some situations.

    And where would we expect it to break down? In its weakest support... the long and short arches.

    Again, thanks, Martin, have a go at this.

    Kevin M
     
  14. Mart

    Mart Well-Known Member

    Hi Kevin

    Great to see an inspired mind getting excited but my initial thought is . . .. . “Beware of getting too carried away with your assumptions”. There are well established ways to proceed with new ideas, and the arena is a great way to expose ideas to be challenged . . . . Implying that you have discovered a new idea that puts others to rest without any convincing evidence which has been largely scrutinized will raise a few eyebrows even if the ideas are compelling. I lay no claim to research experience of any consequence but many readers of these posts can and they will likely expect this approach before taking your claims too seriously. Also there is a trap which is hard to escape from when an idea grabs an inspired mind which drives it to prove it’s idea is correct rather than simply test it and be prepared to see it discredited, there are plenty examples of well respected and seasoned researchers falsifying or disregarding evidence to support their cause and if you invest a lot of effort into an idea it must be pretty tough to have to find that you were wrong.

    Anyhow nuff said about that but I suspect you will see why I mention this. If you did not notice there is an interesting thread current which probes around this issue.

    http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=11338

    I do not understand why you think that the windlass doesn’t provide autosupport because the plantar fascia subdivides distally. Even if there is a differential stress on the different slips and their contribution at any given instant varies I would estimate that the sum of the individual tensile components would remain fairly constant irrespective of frontal plane alignment simply because once the heel comes off the ground the entire body weight has to be borne under the metatarsal heads. Stress and strain of the plantar fascia will vary according to an individual’s walking speed, terrain, foot morphology, things which may encourage or impede progression of COM over the foot and many other issues. I agree that foot-wear may moderate stress but again this is a huge generalization. I agree that reverse engineering biomechanical structures and considering evolutionary advantage is worthwhile but not sure I really understand your deductions.

    Perhaps it would be helpful to explain what you are doing with the cadaver you mention and what your research approach is. There are better read and qualified contributors than me who I am sure would be happy to critique your approach if you give them a bit more to digest.

    look forward to hearing more

    Cheers

    Martin


    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
    Last edited: May 9, 2008
  15. David Smith

    David Smith Well-Known Member

    Hi Kevin M

    Good to see you posting again. Now I know you've been working on cadaveric foot disections for some years now and your anatomical knowledge is highly reputable. However your post has me confused.

    The plantar fascia is a contributor to the intergrity of the plantar vault but not the major tensor. If we look at the material properties of PF it is not possible that it has the capacity to withstand the tensile plantar forces, generated in every day ambulation, on its own.

    Lets assume (from research that I have done) that the PF has a Young's Modulus of aroung 600MPa. The max cross sectiona area is 30mm^2. A normal tensional force required to stabilise the plantar vault of a 100kg man can be >2000N. So using the engineering equation e = S /E (e = strain S = stress E = young's Modulus) then the total strain would be around 0.12mm/mm. The length of PF on a size 11 (49) foot is around 190mm. Therefore change in length, without considering change in cross sectional area would be 22mm, and considerably more if you do consider reducing CSA. The normal change in length of the PF is around 5mm. The Ultimate tensile strength of PF is about 45 - 80Mpa and the its elastic limit at 63% of this. Using the above figures the working stress would be around 70Mpa so failure would occur every time we walked.

    It is my opiion that the PF plays a dynamic balancing role in the intergrity of the plantar vault one which is akin to muscular action rather than ligament action.
    As is common with muscles the PF has a primary and secondary role that changes dynamically throughout the gait cycle. Primary and secondary in this case does not denote greater and lesser importance. It is my opinion that the ligaments with a far higher stiffness than the PF and muscles / tendons, possibly an E up to 1500MPa, solidly secure the rearfoot to midfoot intergrity. While the muscles and PF interact to secure the midfoot to force foot integrity. They can have a secondary role in the support of the rear to midfoot structure in so much as they protect the ligamnets from over loading and can add dynamic support if the ligamnets become lax EG thru plastic deformation or traumatic injury.

    I think this give the foot the dual ability of adaptabilty and rigidity that you speak of. The rigidity of the bones of course give the structural design strength but because of the multpile joints they cannot maintain dynamic stability. The foot in this sense is not a stucture but a mechanism, it is easily deformed by external forces and can only be stabilised by dynamic internal force interactions that resist those external forces. It is designed to adapt and remain stable, within its constraints, simultaneously. Therefore to attempt to attribute stability at a single point in time to a single or a few anatomical components in the foot, may have to be approached with caution.

    Synergism of Anatomical components. I thought this was your thing Kevin IE look at the body as a whole, as the sum is greater than the individual part and it is very difficult to seperate out one component and say with certainty that it has a single purpose.


    How do you mean they cross (PT and PL)? I agree that PL tightens the curve of the proximal transverse arch but wouldn't the PT tend to open the curve. Do not the PL and PT both act to increase MLA height and increase its rigidity. Where is the sling effect?

    It does'nt, They work together, not in seperate actions. Frontal plane load is not about one single joint, althought isn't the STJ the one that tends to be the most traumatised. When foot longitudinal axis moments loads are high we sprain the medial and lateral ligamnets. As I said above the PT and PL also increase rigidity and height of the MLA.


    .

    In this case they become very stable in one direction because the CCJ is screwed together and it is uncommon for the combined forces of GRF and body weight to be acting directly opposite each other as in your scenario. Usually there will be some kind of force couple that will tend to produce moments and lateral forces that will turn the bony structure into a mechanism supported by dynamically reacting sub structures IE muscles tendons PF and Ligaments.

    The foot structure can be compared to an arch but it is not a bridge and such analogies while useful must be recognised for their limitations. The foot does not have fixed loading points, the loads are highly variable and have complicated loading vectors. The structure is a series of vaults that change relative to themselves and each other. Trying to apply one force in one direction onto a predetemined fixed morpholgy and making a conclusion about its structural integrity thereof could be misleading in my opinion. One might conclude that this is therefore the ideal foot shape and try with an intervention to maintain that shape. Whereas that particular morphology is perhaps only useful, in terms of structural integrity, at very limited tempo-spatial moments within the gait cycle.

    You may be right here but this also may be akin to saying that orthoses weaken the arch structure (ala Prof Rothbart)

    That may be true since they are mostly protected by the least stiff structures and have the potential for the greatest deformation and the relatively highest moments.

    If you use a lever to shift a heavy rock you wouldn't expect the lever to break near to your grip.

    All the best Dave
     
  16. kevin miller

    kevin miller Well-Known Member

    Martin, David,

    I knew I would draw fire from that last post. At least it is friendly fire. :good:

    Martin, I think David said it for me when he explained his results with study of the plantar fascia. It simply doesn’t have the tensile strength to handle day to day stresses alone. As for its function at a given time during gait, the slips shorten as the windlass cranks, taking away the Mets ability to float. Just at the end, before toe off, when the foot needs it most, everything is in play. David, please understand that I have always thought this way about the PF….as you point out later…..but I have seen posting the other way here, so I thought it only prudent to mention it.

    David, you got me on being a tensegrity freak, but this is exactly what I am alluding to. The body functions in layer with every component having multiple functions. Off the top of my head I can't think of a structure that doesn't have multiple functions. This is what I am saying about the PT and PL – PB and AH. When they cross each other or in the case of the PB and AH, the double joints, and the chain closes when the heel sits the ground, their function changes. All I can tell you is when I test this over and over and I get the same result, all of the arches increase or decrease their diameter; however you want to put it.

    It does'nt, They work together, not in seperate actions. Frontal plane load is not about one single joint, althought isn't the STJ the one that tends to be the most traumatised. When foot longitudinal axis moments loads are high we sprain the medial and lateral ligamnets. As I said above the PT and PL also increase rigidity and height of the MLA.


    Since my statement was rhetorical, obviously we are close on this, however, I don’t think we really understand the STJ. If it is so traumatized, why don’t we see a lot of arthritis in it? I have two very interesting specimens. One is of a lady who had terrible acquired flat foot, and the other is a dry specimen that was flat footed for so long that the bones themselves changed positions slightly. The STJ in both is pristine. In fact, I have never seen STJ arthritis in a specimen. The only caveat to this is in acquired flat foot they do get arthritis on the edges where the joint contacts, but NOT on the articular surface. This really explains how I can manipulate an STJ and get instant results. I unscrew the joint as you describe them as being in your next point.

    As for orthoses……. You know, I do think some weaken the foot. If they don’t make the foot work, but act more like a splint, they may very well weaken the foot. What do you and Martin think?

    Lastly, while I made the statement about changing the way we think about the foot to draw fire, what David and I have been doing the past few years is, in fact changing things. David has published more of his work. I tend to over analyze…at least that is what I have been told lately, but I this forum there are a umber of people who are bringing new ideas to the table with data to back it up. What say you?

    Kevin M.
    :drinks
     
  17. Mart

    Mart Well-Known Member

    Hi Dave and Kevin

    Kevin, I am glad I did not offend you, when I pressed the send button I was a bit reticent in case I gave the impression that I was some kind of pompous prick stating the obvious so I am glad now you did not seem to feel that , . . . . . . :)

    Interesting to get some detail from your research findings Dave.

    You say

    “It is my opinion that the PF plays a dynamic balancing role in the integrity of the plantar vault one which is akin to muscular action rather than ligament action.”

    Is this because the visco- elastic properties of the PF are more akin to muscle than ligament, because of the "pseudo contactile" shortening from the windlass during late midstance or some other mechanism which I am unaware of ( I have read of contractile elements being identified in the PF for example)?

    I have read some interesting ideas which look at the evolutionary forces which might explain the fact that we have a 3 segment lower limb (as opposed to 2 or something else) and nicely explain the ratio of the human segment lengths based on comparing finite modeling of multiple scenarios and looking at the functional implications for gait efficiency, stability and risk for injury. This is tied in with the idea of “mechanical intelligence” which may operate to predetermine the myriad of coordination tasks and protective limits which give us evolutionary advantage. This line of investigation being distinct from seeking complex peripheral/spinal level neural pathways which are sought as notions of gait patterning generators which anther explanatory route to take.

    Kevin M I get this impression you are thinking along these lines and am intrigued about you cadaver findings. I realize that examining the 3 segment lower limb is probably an easier model to define than a foot but I am curious Dave, given your depth of research on this subject if you have any insights in this direction, hope that makes some sense?

    cheers

    Martin


    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
    Last edited: May 10, 2008
  18. Mart

    Mart Well-Known Member

    Hi Kevin

    For sure I was surprised and interested in David’s results and keen to see more about how these measurements and calculations were arrived at. I have read a bit on tensegrity but cannot get my head around a completely cohesive model of how this could describe a model of foot function. I am presuming your model subdivides the foot into multiple connected integries and that joint compressive forces then represent the connecting boundries. My understanding of true integrisity is that the rigid member framework as you put it ‘floats’ within the supporting connecting “tensile” structures but my understanding of foot skeletal structure is that there are obvious signs of compressive forces acting through the joints. How do you reconcile the multi joint tensile structures of which there are many, perhaps this is my confusion with your idea. I find your observations regarding abscence of STJ degenerative changes intersting, I had never considered this but when I think about it can only recall instances of acute traumatic STJ arthrosis, I need to think about this a bit more! Perhaps I am being pedantic regarding my understanding of the accepted definition of tensegrity but perhaps you could comment on this point.

    As far as foot orthosis are concerned, I agree that there is a good argument to suspect that there may be negative effects such as muscular weakness developing when used inappropriately, I argue this with pts on a daily basis who demand FO from me simply because they have had someone prescribe them before without any reasonable rational to do this.

    Interesting subject; I would really appreciate, if you have time, if you could break down your thought process a step at a time perhaps from initial contact to toe off, defining your boundaries and how the "floating" fits together, this would be a bit arduous but helpful. Perhaps you are so familiar with your idea that it is difficult to understand why someone like me, who has not gone through your experience might have difficulty getting a handle on your reasoning. Perhaps I am being a bit dim and as before I hope you take this in the spirit I am intending of trying to improve my own knowledge not to be nitpickinly critical of what you are seeing

    Cheers

    Martin :drinks

    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
    Last edited: May 10, 2008
  19. David Smith

    David Smith Well-Known Member

    Martin


    No not visco elastic properties, but the windlass action, which is not only working during the propulsive stage of gait as some might imagine.
    During the swing phase of gait the PF is, to all intents and purposes, an extension of the long toe extensors. While the EHL and EDL are contracted the MLA and plantar vault is held in a relatively shortened position. At heel strike to toe contact (somewhere in early midstance) the extensors, in eccentric contraction, still control the tension in the PF. At this point the extensors switch off and are quiet until late propulsive stage. During the time from toe contact to heel off GRF is resisting further plantarflexion of the toes.The plantar plates of the lesser toes come into play and together resist the tendency of the plantar vault to extend and flatten. The part of the plantar vault that is under the influence of strong plantar ligaments does not require the PF to support it and here the PF tensile strength is a back up. However the distal vault from the distal midfoot joints is not restrained by strong ligaments and this part relies heavily on the plantar aponeurosis in which I include the muscles. At heel off the windlass action as we commonly know it, comes into action and draws the rearfoot toward the forefoot and at the same time supinating it.

    This is not new of course but you can see that this action of the PF from open chain to closed chain gait cycles is far more active in foot action than any ligament could hope to be. The ligament has only the characteristics of its tensile strength and elastic properties to influence its far more passive role in joint control.

    Kevin


    I'm glad to see you haven't capitulated on the tensegrity thing.
    I have recently read some interesting article on evolution. They made the point that evolution doesn't progress to the optimum level for that organism only to a level necessary to ensure survival of the species. EG the Zebra did not evolve with a flamethrower to kill predators even tho they have many. Their survival skills in terms of a species was sufficient at running away and so that was all they got. Might this be the same with tensegrity. Obviously the body consists of soft tissue in tension and bones in compression, with some exceptions ( in the general opinion). However to survive as a species we didn't need to evolve to full tensegrity since the current design is good enough.

    Kevin and Martin we don't really want to get onto a tensegrity discussion do we as it was discussed in great detail in previous threads.

    When talking about the STJ I was referring more to its extrinsic supporting tissues such as ligaments and capsule. However we often see the STJ in a fixed or limtus position.

    New ideas are great, they challenge our boundries, stir us out of complacency and stimulate debate and critisism.

    All the best Dave
     
  20. kevin miller

    kevin miller Well-Known Member

    Martin, David,

    I am sorry for confusing you both about my views on Tensegrity theory. What I am doing with the foot at this point is breaking the complex layering of tensile and compressive structures into manageable components. As I mentioned to David in my last post, the human kinetic chain appears to be composed of layers and layers of structures which have multiple functions. With that, let me try to clear things up.
    I am presuming your model subdivides the foot into multiple connected integries and that joint compressive forces then represent the connecting boundries. My understanding of true integrisity is that the rigid member framework as you put it ‘floats’ within the supporting connecting “tensile” structures but my understanding of foot skeletal structure is that there are obvious signs of compressive forces acting through the joints. How do you reconcile the multi joint tensile structures of which there are many, perhaps this is my confusion with your idea.
    As I mentioned, the subdivision of the foot is done to simplify the Tensegrity model. Force transfer throughout the kinetic chain remains the same -- any input in any place instantaneously affects all other components. The difference between Bio-Tensegrity and structural Tensegrity is that the elastic tensile structures of a biological system allows for transient contact of joint surfaces. Transient is the key. If there were more than moment contact on articular cartilage, it would quickly wear down and produce arthritis, just as we see with a pathomechanical foot.

    I find your observations regarding abscence of STJ degenerative changes intersting, I had never considered this but when I think about it can only recall instances of acute traumatic STJ arthrosis, I need to think about this a bit more! Perhaps I am being pedantic regarding my understanding of the accepted definition of tensegrity but perhaps you could comment on this point.
    I really can't see much different and any other aspect than the joint surface contact variation. One more comment on that: There are no flat joints. Every joint has some variation in topography which means that as the joint goes through its range of motion he instantaneous contact point provides relief from pressure to the areas around it. So, even as joint contact is transient motion within joint motion produces transient contact as well. An interesting bit of trivia here; mechanoreceptors in and around joins measure this force and try protect both the cartilage and ligaments. This even occurs when you're lying down at night during sleep. We roll around are shift every 15 to 20 minutes at minimum. It is interesting that a stress-strain curve of ligamentous tissue shows that low stress will produce strain and about 20 minutes. David may want to comment on this.

    Interesting subject; I would really appreciate, if you have time, if you could break down your thought process a step at a time perhaps from initial contact to toe off, defining your boundaries and how the "floating" fits together, this would be a bit arduous but helpful. Perhaps you are so familiar with your idea that it is difficult to understand why someone like me, who has not gone through your experience might have difficulty getting a handle on your reasoning. Perhaps I am being a bit dim and as before I hope you take this in the spirit I am intending of trying to improve my own knowledge not to be nitpickinly critical of what you are seeing

    This is a difficult one. Because it appears to be a Tensegrity structure, everything that happened in the foot affects the rest of the kinetic chain, and within the foot itself each structure has multiple functions, often occurring at the same time. Explaining these functions without diagrams is practically impossible, but at worst I can only confuse you more. So let's give it a shot.
    The foot acts like a 3 point leveling mechanism to adapt to constantly varying substrate topography. At heel strike the entire forefoot is floating. (I use this term because it is easy to visualize.) The ankle stabilizing muscles are certainly functional, but the midfoot stabilizers have not fully kicked in yet. At fifth ray contact, we begin to see the four muscles we have been speaking about, posterior tibialis, the abductor hallucis, the peroneus longus, and peroneus brevis, begin to fire in earnest.
    Compression of the lateral column causes the CC joint to activate. There is a very complex sequence of events that occur right here but it would take pages to explain. Suffice to say that the lateral column only becomes finally stable when the fourth ray contributes to the stability and the superior medial process of the calcaneus and the superior medial lip of the cuboid make contact. Even now the medial column remains mobile enough to adapt. As the Center of pressure begins to move across the foot, a group of ligaments are rarely spoken of call the intertarsal ligaments or the internal tarsal ligaments increase tension. This pulls the medial column and lateral column into alignment and forces the lateral cuneiform into a notch between the navicular and cuboid, finalizing the stability of the medial and lateral columns. As the first ray begins to bear weight, a properly positioned series of joints stabilize the foot from within, requiring little input from supporting soft tissues. What I am suggesting here is that the soft tissues align the bones just prior to weight-bearing so that the bones can bear the weight for the body, transmitting force through the most dense tissue which is more efficient, and which also protects the soft tissue. Anything that causes the aligning musculature to get out of sync will produce a weak point in the kinetic chain breaking the egg, so to speak.
    I hope this helps a little bit. If I did not address exactly what you would like me to, please feel free to ask a pointed question.
    Regards,
    Kevin
     
  21. Kevin Kirby

    Kevin Kirby Well-Known Member

    Folks:

    I am reading again about this biotensegrity stuff that I thought, in our earlier lengthy debate on tensegrity, most of us concluded could not be applied in the human foot since the joints of the foot and lower extremity are under compression for long periods during all weightbearing activities. Tensegrity models do not have compression forces at their joints. There are much better ways of modelling the internal and external forces throughout the foot and lower extremity that does allow compression forces through the joints of the foot and lower extremity than using "biotensegrity". Please, let's discuss these interesting subjects in terms of scientific reality, not scientific fantasy.
     
  22. kevin miller

    kevin miller Well-Known Member

    I have recently read some interesting article on evolution. They made the point that evolution doesn't progress to the optimum level for that organism only to a level necessary to ensure survival of the species. EG the Zebra did not evolve with a flamethrower to kill predators even tho they have many. Their survival skills in terms of a species was sufficient at running away and so that was all they got.Might this be the same with tensegrity.
    I think you are right here David. This almost has to be as with other cases within the body such as the wisdom teeth.

    When talking about the STJ I was referring more to its extrinsic supporting tissues such as ligaments and capsule. However we often see the STJ in a fixed or limtus position.
    Thank you for bringing us back around. The fixed position of the STJ is exactly what I was writing about in an earlier post. In my cadaveric studies I have found that the STJ has very limited movement. I think that we have, as a group, possibly misread some of Manter and Hicks work. They described the inclined plane of the STJ which should have been a hint its motion is limited to about one half the radius of the "bowl" the talus sits in. More profoundly, the transverse ligament is extremely thick and encompasses the entire diameter of the talus at this level. To have more than half the radius of the bowl would require that this ligament rotate upon itself lengthwise. This just isn't going to happen. My measurements show that the ratio of movement is about .4 and rotation and a bit less than that in anterior and inferior motion. Rotating to its endpoint, the STJ grinds itself down like to wires twisting upon each other. The edges of the STJ began to touch and compress the articular cartilage. This is why I mentioned earlier that the only arthritis I can find in an STJ is and the edges where the STJ has been fixed for some time. Perhaps referring to it as the limits is position is appropriate as well because I can "unfix" the joint with a simple manipulation. In summary, because of the lack of motion and evidence demonstrated when the STJ becomes fixed, I would say that we are going to have to look more towards the midfoot for correction of the foot with orthotics. Of course, I am not the first to say this neither will I be the last. Hopefully, I can just help tease out the answer.

    Cheers gentleman,

    Kevin M.
     
  23. kevin miller

    kevin miller Well-Known Member

    I'm sorry, Kevin, if we offended you. Please tell me what part of what Martin, David or I wrote is fantacy and I will make sure you never have to read it again. By the way, is that the collective "we" or the royal "we" that determined that tensegrity models don't account for compression. If you read closely enough, you will see that this topic was indeed clarified.

    Regards,
    Kevin M.
     
  24. musmed

    musmed Well-Known Member

    Dear All

    Hi, I would like to add something that has been missed and as far as I am aware has not been mapped unlike the role of the fibrous diamond of the trapezius muscle between the shoulders at between C7 and T2-3.

    As I stated in many a post the biceps femoris is a foot muscle. This is an embryological fact. Look up Larsen's book called 'Human embryology' for the details.

    The biceps femoris has many a role from acting on the knee to everting the calcaneus so as to stabilise the subtalar joint and keep it in neutral. This action is one of sidebending the joint.

    The second most important feature of the biceps is the action it places upon the interosseous membrane.

    When one mobilises the superior and interior tib/fib joint there can be up to and over 1cm of joint translation in an orbital plane at both joints.

    The reason for this is so it can change the angles of the interosseous membrane. In doing so has an affect on any muscle that is attached to the membrane.

    For those who are lost:
    Think the interosseous membrane as the dorsal fin of a fish.
    When it is collapsed it is pointing towards the fishes butt, but when it is active it is pointing towards the sky.
    Thus the direction of its action (ie. pull up the dorsal spines) has changed.

    Now imaging you are looking from behind the leg, through the tibialis posterior to the interosseous membrane when the biceps femoris is not very active.
    Here the fibula is 'relatively down' ie not being pulled up and thus the posterior tibialis muscle fibres are attached at almost a horizontal position.

    The tibialis posterior muscle can still fire and function.
    When the tibialis posterior muscle is firing and shortening
    and the biceps femoris is firing
    This action can not only assist the tibialis posterior's action (power. A bit like you pulling a rope and some one behind pulls your waist. They do not contribute to the rope directly), but also the DIRECTION the fibres are pulling.

    This synergistic action not only can strengthen a muscle directly by "pulling upon it" but also CHANGE the direction that the Post. Tib. muscle exerts its force.

    What a brilliant controlling mechanism in 3 planes. The shoulder works the same way. That is why we do not break things (bones/muscles/Ligs/etc) more often.

    This is what we call fine tuning.

    Regards
    musmed coming to the UK!
    www.musmed.com.au
     
  25. musmed

    musmed Well-Known Member

    Dera Kevin

    I am at a loss here. Who were "most of us". Just been through all the last several hundred pages and i cannot find the 'most of us'.

    Anyway.

    The foot joints are not constantly under compression for long periods during weight bearing activities. Whenever something is NOT right we move, even though it may be just a 'tad'.
    This 'tad' is just enough to offload the most annoying discomfort.

    Think of sitting on a hard seat. Initially you ignore the discomfort. Eventually it occupies your brain... you move a 'tad' and the pain/discomfort is instantly gone.

    Each one is a specialist at doing this....

    Try this for tensegrity.

    what happens to the tenocyte when it is put into growth medium so as to try and grow cultures of tendon.
    prof Khan from the famous book Brunker and Khan fame on Sports Medicine has found out that the tenocytes that sit between tendons and look like cigars once in a growth medium become spherical as all cells do no matter from what part of the body they come from once placed in a growth medium, ie outside of a tensegrity system.

    May I suggest that maybe some ideas that may seem outside the norm be looked into before the idea is shut out by a major voice.

    If you care to study the life and time of Sir William Harvey the discoverer of circulation. it took almost 100 years to believe him and he spent most of his adult life inside the catholic churches sanctuary so he would not be burnt at the stake as a heretic .

    You can find his name in churches in London just the road from london tower and at Durham catherdral near Newcastle on Tine.
    Regards
    musmed
    Paul C
     
  26. Mart

    Mart Well-Known Member

    Errrm . . . it is Sunday.

    I am feeling a little bolder and more mischievous than usual. I had great success this week, persuading a skeptical local farmer that trimming his keratoma with a welders cut off wheel was a akin to slaughtering a chicken with a burst from semi automatic.

    I am intoxicated with confidence and sneek onto the pod arena pulpit whilst the preacher goes for an quick whizz before delivering the passionate final inspiration . . . . fire and brimstone are in the air . .. . .

    “Fellow podarenarists, as you may have realized I am a woosy Canadian who loves and hopes to be loved by everyone (except intolerant bastards who don’t know their ah from a hole in the ground).

    I propose .. . . . how about inhibiting that hard wired primitive part of our brains which gravitates towards tribalism and since it can be fun to duke it out intellectually keep the duking fun and not personal.

    Since I came across it the maxim “Nothing is more likely to impede investigation than the premature acceptance of an explanation” it seems to ring true for me on a daily basis . . . . . .. so long as I am not in too much of a hurry.

    People of course have different levels of acceptance, knowledge, experience, and patience for those of us who need to regurgitate their diet a little. I am more of ruminant than a carnivore so I guess it is easy for me to feel this. . . . .

    . . .. . Let us prEy”

    Before being dragged from the pulpit for being banal and heretical I rejoin the congregation.


    Paul you said


    I cannot see how you arrive at this, which joints and when are not under constant albeit varying amounts of compression when weight-bearing?


    Also you say

    Sorry for being dim but I just don’t get your point here please chew the cud if you have a minute.


    You said

    This may be true, but it doesn’t seem like a good argument to believe things just because the church rejects it.

    I need to go think about David and Kevins posts a bit more

    cheers


    Martin


    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    Phone [204] 837 FOOT (3668)
    Fax [204] 774 9918
    www.winnipegfootclinic.com
     
    Last edited: May 11, 2008
  27. Mart

    Mart Well-Known Member

    Kevin

    I do not understand your point here. I agree that David may have demonstrated that the PF is incable of withstanding the strain induced by weight-bearing foot on its OWN without injury and if true it is good that he has taken the trouble to demonstrate this in his work. Since normally the PF functions well, a compreshensive understanding of the other structural influences is important too. This is why I am particularly interested in this thread.

    So the implication may be that if the supporting structures which normally protect the PF from injury fail this would lead to PF injury which appears to be a common problem.

    My understanding is that the primary accepted role of the windlass is to configure the middfoot to encourage their joint compression forces in a way that relieves the supporting structures especially during late midstance and when this fails the other supporting structures become overloaded and the articular surcaces of the joints likewise overloaded.

    I do not see how the metatarsals can float and be part of a load bearing structure or why if they were truly floating their structual morphology would not suggest this.

    Please point me in the direction of another thread if this has already been dealt with elsewhere

    cheers

    Martin


    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
  28. kevin miller

    kevin miller Well-Known Member

    Since I came across it the maxim “Nothing is more likely to impede investigation than the premature acceptance of an explanation” it seems to ring true for me on a daily basis . . . . . .. so long as I am not in too much of a hurry.

    LOL…… this sound and like something Paul would say. To that end, he flew all the way from Australia to the United States just to see if I was holding my head under water to long on these very topics. So if I get support from Paul, either he believes it or he is trying to justify his plane ticket.

    So the implication may be that if the supporting structures which normally protect the PF from injury fail this would lead to PF injury which appears to be a common problem.

    My understanding is that the primary accepted role of the windlass is to configure the middfoot to encourage their joint compression forces in a way that relieves the supporting structures especially during late midstance and when this fails the other supporting structures become overloaded and the articular surcaces of the joints likewise overloaded.


    Please point me in the direction of another thread if this has already been dealt with elsewhere

    I know of no other posting on the website. But what Paul and I are both saying is simply a review of physiology. Cartilage covers bone and stays alive through transient compression which nourishes it through osmosis. If too much compression is borne by the cartilage, the fluid is compressed out of the cartilage and arthritis can occur. So, bone does not make contact, articular cartilage does - and only transiently. Paul mentioned that joint surfaces are full of mechanoreceptors which do not allow you to maintain damaging pressure on any one point of the joint surface, and joint surfaces are relatively uneven or curve so that a slight movement dramatically shifts pressure. This happens in all compressive joint.
    I do not see how the metatarsals can float and be part of a load bearing structure or why if they were truly floating their structual morphology would not suggest this.
    The the rear foot and midfoot as being locked while each metatarsal functions only short ROM hinge. Each has only a few degrees of range of motion in the sagital plane and rocking the forefoot in the frontal plane allows each metatarsal head to move within its narrow range of motion. This is the floating speak which allows the forefoot to instantaneously adapt to any surface variation.
    I hope this helps I am not sure that I am saying the right thing.
    Kevin M.
     
  29. Stanley

    Stanley Well-Known Member

    I was at a seminar where Sammarco gave a lecture on joint mechanics. He said that a molecule of glucose would take months to get into the deeper layers of cartilage if it was left to Brownian motion alone. He then went into a discussion about the pumping action of the cartilage with motion. He also discussed how an abnormal progression of the instantaneous center of motion of the joint is responsible for arthritis.

    Regards,

    Stanley
     
  30. kevin miller

    kevin miller Well-Known Member

    Exactly, Stanley. Good to hear from you.

    Also, Martin, I woke up thinking aobut what I said concerning Met floating. That floatation is what occurs at late midstance, when everything is begining to really tighten up, but the Mets still have some length on their slips. Once the windlass takes up the extra length.... and it is not really a windlass. A windlass has a round axle, the toes have progressively larger cams, ending with the super-sized cam of the great toe which shortens the long arch and pulls the rearfoot into varus......once the extra length is taken up, the toes become rigid as well, at LATE toe-off, meaning the foot remains adaptable to a small degree right up until the end. Where would this come in handy? Running barefoot over soft ground. It "mushes" out as you step. Running through this requires adaptation as it compresses. Lastly, toe running still needs some adaptation, to surface topography, even if for a brief period.

    Regards,
    Kevin M.
     
  31. musmed

    musmed Well-Known Member

    Dear Martin

    It's not just Sunday, it MOTHER'S day (or was).

    The church was not were I was aiming, It was the medical profession. Sir William Harvey took sanction in the church so that the church could not cook him for heresy!

    The medical profession is always late. Have you not noticed this, ever?

    The foot has two components. One for standing and one for everything else. Your foot will only hurt in standing if you are on the wrong side of the foot (ie everything else) and vice versa.

    Thus very little of the foot is in contact with the ground. The system pulls the joints together and this action makes the cartilage take up the 'slack' between joints and thus no bone on bone compression exists and thus no bony compression occurs and thus nothing hurts.
    When the cartilage is looking for nutrition you move, this allow the cartilage to take some nutrition and then back to where the system is in its neutral.
    Have you never had an ache in your bottom when seated? Eventually you move that tiny bit and instantly the pain or discomfort has gone? This is how we survive in a gravitational field.

    As far as the tenocytes are concerned. I hope there are others out there wondering why I put this in the arena.

    We exist by gravity pulling upon us. We have had a eon of time to adapt to this 'force' or what ever it is, just gravity.

    I love it when you hear about what caused the dinosours to die and disappear.

    There are many theories about from volcanoes to meterorites, agree?

    In the mainstay of Newtonian physics says gravity cannot vary, but it can.
    So an acute change in gravity over 2-3 million years gets rid of the dinosours they go to the water to survive, hold up their weight, the 400 foot trees in California disappear, under gravitational pull the waters head towards the poles and thus compression of water into ice, this causes the water to recede from land and the dinosours not only become smaller and water dweller but the big ones die out.

    BUT most importantly, the quadrapeds can become bipedal and thus us...

    So what is this all about.

    I mentioned the tenocytes, you wrote what is this all about, so I will tell you.
    Whether or not you believe in tensegrity, have a think about this.

    You have heard about the painless rupture of the Achilles eh? ever thought why?

    Here is the answer:
    When tensegrity breaks down things change for the worse.

    If you look at an ultrasound of an Achilles tendon with holes you can say that the holes are due to dead cells and thus nothing (maybe fluid) is there.

    But when samples are taken and stained they show a different picture.

    The holes are areas of necrosis, (dead cells) but there are also areas of fat, almost circular , blue staining cells.

    How did these arise.
    Macropharges can be almost any ground substance cell, from a tenocyte to a chondrocyte.

    Hypothesis: tension is the governing structure word for human (and probably all other cells)
    once this is removed, ie no tension then the only possiblity is compression..

    so these tenocytes change their nature and become primitive chondrocytes and lay down primitive cartilage (blue staining) in the tendon.

    Bingo, we have a painless rupture, simply because we replaced the tensioned tensegrity system with a compressive one.
    I am certain you will agree that you cannot put a compressive element inside a tensile structure, but this is what happens.

    Hope your religious thoughts are not too non contiguous after reading this, especially on Mother's Day.

    Regards

    Paul Conneely
    www.musmed.com.au
     
  32. David Smith

    David Smith Well-Known Member

    Mart

    You wrote
    Two things here, First I am not saying that because the PF apparently is not strong enough to withstand alll the tensional load of plantar vault extension therefore tensegrity must exist. I have listened to and read much about tensegrity and still cannot see it in it pure form in the anatomy of the body.
    I believe that Newtonian mechanics give us the tools to explain the actions of the body adequetly. However while it would be very nice if tensegrity did exist I do not have the inclination to persue that avenue of thought. I do think it is very handy that Kevin does persue his passion with biotensegrity and maybe one day he and others in that field will be able to put together some convincing evidence.
    Secondly from my research experimentation I have indentified some PF mechanical characteristics. These have been consistent with findings of others such as Hicks, Kitaoka, Carlson, Gefen, Stansfield and others. By correlating these findings and using X ray and MRI meausrement for PF parameters then engineering theory to calculate stresses within the real PF it appears that it is not possible for the PF alone to withstand the sum of tensile forces applied. However there are extremely widely varying material properties values attributed to the PF by researchers from different disciplines, which make further research in this area necessary to confirm this theory.

    I believe tho that the PF, almost alone, protects the SLC from overload and plastic deformation. This is because when the windlass is operating correctly it shortens the lever arm vailable to increasing GRF at the propulsive phase and therefore reduces internal plantarflexion moments about the TNJ required to resist external dorsiflexion moments of GRF. The SLC is a major contributor to internal plantarflexion moments about the TNJ and therefore is protected from overload. The lever arm avialble to the SLC to produce plantarflexion moments about the TNJ is very small therefore there it is reasonabl to assume that there are potentially high internal stresses in these tissues. The SLC ligament tissue is very stiff compared to the PF for instance and small increases in strain will result in relatively high increases in stress. It is desirable therefore that the SLC is not highly strained. The correctly operating windlass achieves this objective IMO.
    Reasearch (cheung Jt, Crary JL, Ward ED) has shown that surgically releasing the PF does not result in immediate or full collapse of the plantar vault. This does however lead to excessive strain on the SLC and over time plastic deformation will allow the MLA to collapse as will be seen perhaps where a ruptured PF is left unattended.


    Cheers Dave
     
  33. musmed

    musmed Well-Known Member

    Dear Dave
    I too like a holiday but never a thinking one that you have just posted.

    I often wonder what the writer is saying when they constantly use abbreviations.

    What is for me and probably those who read these comments and never reply simply because they do not know what is written about.
    May I be so bold to say that before we forgo tensegrity, we forgo abbreviations.

    So: what is SLC and TNJ for starters?

    Thanks in reply. Notice it is in english?
    Regards Dave
    Paul C
    Remember the eye will only see what the brain allows....
    Dave the Plantar Fascia has nothing to do with anything other than
    1. control of the subtalar joint
    2. gasctocnemius power transfer to the MET (metetarsal heads) at and beyond heel off.
    3. the Plantar fascia does not support stationary standing. If it did you feet would perish very easily and quickly.
     
  34. kevin miller

    kevin miller Well-Known Member

    David,


    I really don't want to get into a tensegrity discussion, but I think there are some terrible misconcetions going on here.

    Your explaination sounds perfectly plausible to me. In fact, I would say that it is part of the tensegrity system at work. Look, I don't have any illusion that "pure" tensegrity theory works for the body anymore than bridge building mechanics does. Pure tensegrity is a building science. It does exist. It has been used since the 50's to build geodesic domes and other similar structures. But understand, these builders think they are taking something from nature and using it to build with. They do not believe they CAN use tensegrity in its most pure form - like it is found in nature.

    It seems the biggest issue is bones not touching. Think about it. They do not touch. Yet, while a builder or sculpter can use longer tensile units and air to keep the compressive units from touching, that doesn't work in nature. We need a way to keep them from TEARING UP or gamaging, not touching. This is the point...... longevity. Enter articular cartilage. Paul, Stanley, and I have already discussed its function. All I ask is that you clear your mind of the ruble that has been built up by people trying to dispute something they know nothing about and think about it. You already know they answer, David. I hear it in a pure form everytime you write.

    Regards,
    Kevin
     
  35. David Smith

    David Smith Well-Known Member

    Paul

    Have you taken umbrige at my last post, perhaps it was this bit.

    There was no veiled critisism here I just require more convincing evidence. In this way I am more of an agnostic than an atheist. I believe in the possibility but not in the truth. But I am happy that there is someone out there looking for that truth.

    Abbreviations, I agree abreviations are mostly confusing, however SLC (Spring Ligament Complex) has been used previously in this post and TNJ is a very commonly used abreviation for Talo Navicular Joint. As is MRI (magnetic resonance imaging) and GRF (Ground Reaction Force), IMO means in my opinion and PF means plantar Fascia.

    The Spring ligament complex as described by Davis WH, Sobel M and DiCarlo EF Foot & Ankle Int 1996
    "It was found there are two definitive anatomic structures that are commonly called the spring ligament: the superomedial calcaneonavicular ligament (SMCN) and the inferior calcaneonavicular ligament (ICN). The SMCN ligament was found to have histologic properties that suggest significant load bearing. The histology of the ICN ligament suggests a pure tensile load function. The deltoid ligament and the posterior tibialis tendon had direct attachments to the SMCN ligament in all specimens".

    Also Morphometric Dimensions of the Calcaneonavicular (spring) Ligament. Patil V. et al F & A int 2007

    "The spring ligament complex (SLC) is a static
    support of the head of the talus and a major anatomical
    contributor to the integrity of the medial longitudinal arch,
    particularly if the dynamic support of the posterior tibial tendon
    is compromised. For this reason, we sought to further elucidate
    the anatomical components and dimensions of this ligamentous
    complex. Methods: Dissection was performed on 30 adult
    cadaver feet disarticulated at the ankle joint that were preserved
    by embalming technique. Results: The superomedial ligament
    (SML) averages 42.51 ± 3.93 mm and 33.44 ± 3.34 mm at
    the superomedial and inferolateral borders, respectively. The
    width at the level of sustentaculum tali and navicular tuberosity
    averaged 20.00 ± 2.35 mm and 10.26 ± 2.05 mm, respectively.
    The medioplantar oblique (MPO) ligament averaged 23.56 ± 2.15 mm and 21.20 ± 1.42 mm at the medial and the lateral
    borders, respectively. The widths at the navicular and calcaneal
    side were 2.71 ± 0.39 mm and 8.14 ± 0.56 mm, respectively.
    The inferoplantar longitudinal (IPL) ligament measured 4.26 ± 0.43 mm and 2.66 ± 0.42 mm at the medial and lateral borders,
    respectively. The width at the calcaneal and navicular insertions
    measured 5.21 ± 0.53 mm and 3.39 ± 0.39 mm, respectively.
    Conclusions: The distinction between the SML and MPO
    components of the spring ligament complex is difficult. This
    study tried to clarify the dimensions and configurations of these
    components of the SLC. Clinical relevance: This effort may aid
    surgeons who wish to repair this ligament with more precision.


    Hope that is clearer for you Paul.


    All the best Dave
     
  36. David Smith

    David Smith Well-Known Member

    Oops pushed send to early.

    Paul to take up on your second part

    1) What ever joint or joints that the Plantar Fascia crosses will be influenced by its internal tensional forces. The Plantar Fascia crosses many joints.

    2) This is one function but a more rigid and fixed Ligament in place of the plantar fascia could do this also.

    3) I don't think I said that it did but it probably does to some extent, in my opinion.
    Often the hallux has very little vertical GRF applied to it during stance and even in the early to mid stance phase of gait there can be low GRF sub hallux. Therefore this part of the PF is not engaged signifcantly for arch support. However the PF slips into the lesser digits are tied also by the plantar plate and this can tension the PF even when there is no GRF applied to the lesser digits. What magnitude of tension this might be is not soemthing I have investigated and I have found no literature that indicates that this research has been done. However since there is GRF applied to the metatarsal heads 2-5 during stance the I would bet a pound to a pinch of dog poo (and I'll hold the stakes in my mouth) that the PF tension is a significant factor in the structural integrity of the plantar vault. The plantar plates would serve little other purpose as far as I can see. Therefore in my opinion the part of the plantar fascia that eventually slips into the hallux windlass is primarily a mobiliser of the foot mechanism, whereas the part that slips into the lesser digits is primarily a stabiliser of the foot structure.

    Cheers Dave
     
  37. Mart

    Mart Well-Known Member

    Hi Kevin

    Have you read Turvey's "Action and perception at the level of synergies"?

    I have had it sitting in my hard drive for a while, I did a quick skim read but not had the impetus to read it (40 pages and lots of jargon, a bit of a brain buster ). I am thinking it would make a good exercise to use this reference to get us to tighten up our use of language and concepts, if you are up for it I would enjoy studying this in relation to the foot and some of the things I think we are trying to understand. If anyone is up for this I can email them a pdf . . . perhaps we could start another thread just to discuss this paper. What do you think? Anyone else read this and doesn’t think it worth the effort?

    Here’s his intro incase you are not familiar with it;

    1. Introduction

    A traditional intuition is that the human movement system is hierarchical, with each level solving a particular class of motor problems in the assembling of an act (Bernstein, 1996; Jackson, 1898; Weiss, 1941). The term hierarchy is used broadly, referring to an organization analyzable into successive sets of subsystems without implying, necessarily, a relation of subordination among them (Jordan & Rosenbaum, 1990; Simon, 1962; Turvey, 1977). In Bernstein’s functional hierarchy, the level responsible for forming synergies of large muscle groups and different patterns of locomotion is referred to as the level of muscular–articular links or synergies. The shape of this level is defined by the central problem of movement control and coordination: The problem of degrees of freedom – the problem of how to compress the movement system’s state space of very many dimensions into a control space of very few dimensions. This compression is the expertise of the level of muscular–articular links or synergies. The coherence, harmony and precision timing of rhythmic limb movements and speech movements typify the level’s special expertise.

    cheers

    Martin

    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
  38. Mart

    Mart Well-Known Member

    Hi Paul

    Thanks for your reply. You mentions lots of interesting ideas. The problem I have is that most of what you say speculative without supporting evidence, so the whole picture you present is based on purely on conjecture. I dont have enough depth to my knowledge to make useful comment on it.

    I am firmly in the Dawkins camp, and as regards mothers day . . . . . I regard this largely as cynical consumer exploitation, how miserable is that? :)

    What do you think about looking at Turvey's paper?

    cheers



    Martin

    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
    Last edited: May 12, 2008
  39. kevin miller

    kevin miller Well-Known Member

    Martin,

    I would love to start a new thread. Standardizing the vocabulary for biological systems has not really been done, so THAT would be a big help. It would help me create a better outline for a paer I am just starting, We would not continue to write about something that is not "function of the spring ligament'" and I am sure that a few intrepid souls will want to participate. You can count on Paul and Stanely for sure and I would really like David to join as well.....if he has the time.

    Just a few questions..... I know there is a way for us to link names and/or subscribe to a thread so that I don't have to check to see if someone has written anything. Can you tell me how to do this? (Stanley was trying to tell me how to use the quotes too, but I have been dictating this on Dragon 9 and pasting it back.) What are you going to call the thread? It isn't really a tensegrity discussion, though tensegrity is involved inherently in the discussion of synergies and ratios of muscle output. If we go down this path, there will be a splatter of neuroscience as well. I see an opportunity to do what forums like this do best...make people think and disseminate information. Just tell me where to go.

    Kevin M.
     
  40. Mart

    Mart Well-Known Member

     
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