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Functional Hallux Limitus, my project so far...

Discussion in 'Biomechanics, Sports and Foot orthoses' started by vegetableplots, Jan 26, 2009.

  1. Graham

    Graham RIP

    Phil,

    I would disagree. I would suggest that the delayed heel lift is likely due to a FnHl. The compensation in these clients with a medially deviated mid tarsal/subtalar jnt axis is to destabalize the MTJ and create a hinge allowing the heel to unweight.

    What we see in many of these patients is the result of their interaction and compenasation on hard flat surfaces, Re" Adult aquired flat foot". over time. The abduction is likely due to their hip ROM, less internal and more External.

    Allowing the first ray to drop and improving dynamic hallux rom is esential, as well as dealing with Midtarsal/sub talar axis rotation, with a Kirby Skive.

    Just a thought.
     
  2. Phil Wells

    Phil Wells Active Member

    Graham

    Back to the 'old chicken and egg' situation.
    However due to the mtjt and stjt axes etc being adaptable/moveable entities as a result of the forces going through them, I believe that FnHL cannot be the prime cause of Mtjt de-stabilisation.
    If you look at phasic movement of the CoM and CoP in the foot, you can definitely see that the midtarsal joint has the potential to be de-stabilised prior to any potential FnHL.
    Those patients with the delayed heel lift that I described earlier often have increased stiffness in the tendo achilles. The first major joint(s) to allow for the CoM to progress over the foot is the Mtjt and where this joint has decreased stiffness or a predisposition towards 'pronation' (e.g. a medially located STjt axis), then an abduction moment will result on the forefoot.
    My own approach is to accelerate the CoP via heel elevation and a 1st ray addition to reduce any potential dorsiflexion moments on the 1st ray. I try and deal with the cause of the need for compensation rather than the pronation moments alone. Medial skives, inverted pours etc are usually used as well.
    However, the concept of an apropulsive gait leading to changes in hip power and possibly the development of an abducted gait are very interesting but do disagree with your theory.

    What do you think?

    Regards


    Phil
     
  3. Graham

    Graham RIP

    Phil,

    which came first? Must be the chicken. Eggs can't ----!

    Probably six of one and half dozen of another. Our theoretical lenses may be diffenet. I hazard a guess that our therapeutic application is very similar. I believe this is the direction Biomechanics and Orthoses will go. We will increasingly be able to demonstarte the effect of these divices with more objective and accurate gait measures.

    We no doubt will always disagree on why and how. what fun!:dizzy:

    regards
     
  4. Bruce Williams

    Bruce Williams Well-Known Member

    Phil;
    I don't discount what your proposal regarding the Midfoot/MTJ adn AJ rom's potentially or predominantly at times leading to FnHL. I do disagree with your anecdotal finding that patients who abduct adn have a pinch callus at the IPJ generally don't have FnHL.

    Finally, just because a patient has a FnHL determined from a physical exam does not mean that all of their pathology derived from the FnHL. Problems can arise in other joints proximal to the mpj's and end up causing a FnHL. I do find that often treating the FnHL primarily, and sometimes singularly, you can eliminate many of these proximal joint problems. I think that this is a very interesting phenomenon regardless of what caused what or chicken and egg!:D

    sincerely;
    Bruce Williams
     
  5. I agree with this statement,

    The patient may have no apparent FHL however, there could be osteoarthritis of the hip not allowing extension or internal rotation thus the patient will have to find a compensatory gait (abduction or swinging gait), this pattern could be causing the callus of the hallux without apparent FHL. Again just another theory.

    John
     
  6. David Smith

    David Smith Well-Known Member

    Howard

    Sorry to take so long to get back I've busy with things and also doing some theoretical biomechanical analyses of the action of Iliopsoas in gait with saggital plane block due to equinus and FncHL.

    Clearly IliosPsoas (IP) is a major flexor of the hip. The origin is in the lumbar spine and iliac crest, both medial to the hip joint, and the insertion is in the lesser trochanter (LC). With the hip in the standard position of reference (Neutral) the the LC is directly inferior and slightly posterior to the hip joint. This means that there are also secondary actions of external rotation and adduction of the hip. This appears to be quite important in the scenario of the analysis of interest.

    First I will assume the stance phase as braking, roll over, propulsion in the three rocker model of heel. ankle, MPJ. In the standard reference gait I assume the braking force becomes insignificant at a hip flexion / extension of +/- 10dgs from neutral.

    This can be seen in a force time graph of +/- Fx (anterior - Posterior Force). At some point on the graph as GRF and body weight force (Fbw) are vertical, equal and opposite, the Fx = 0.

    If we look at the same force time graph for a gait with saggital plane block due to ankle equinus and FncHL, then the area under the curve relating to +/- 10dgs is much greater than for the reference gait, indicating a greater force impulse. The main feature of this portion of the graph is the sudden steep change to and from the zero Fx. This indicates a sudden deceleration (or negative acceleration) of the CoM and therefore a sudden increase in the inertial force of the CoM and particularly the HAT (head, arms and trunk) CoM.

    This then will lead to a sudden tendency to hip flexion at the same time, if we assume a compensation or primary action (chicken and egg but lets not argue here about detail) of STJ pronation, there will be an internal rotation (int rot) of the tibia, knee and hip. Hip flexion reduces IP tension and hip int rot will increase IP tension. Lets assume that the hip does not actually flex due to antagonistic actions of hip extensors. In this case saggital plane block (SPB) will tend to increase hip extensor action and so in the above scenario IP tension will increase here compared to the gait of reference.

    At this point the CoM has reached a low point in velocity, in the reference gait a graph of the velocity over time will ideally show only a small change in amplitude. In the SPB gait the sine wave will show a great change in amplitude. Therefore in order to maintain and equal average velocity compared to the reference gait the SPB gait wil have to increase acceleration at propulsion.

    If this assumption is correct then push off force in the SPB gait must be relatively increased. This will cause an increase in HAT CoM acceleration and inertial force. The inertial force of the HAT CoM will tend to extend the hip and therefore increase tension in the iliopsoas. The IP will now tend to resist hip extension but also assist hip external rotation (ext rot), which is excessively internally rotated and resisting ext rot due to FncHL not allowing the engagement of the windlass and assisting with resupination and ext tibial rot.

    It would appear, using these assumptions that there could therefore be two peaks of IP action during the stance phase of gait in the ipsolateral leg.

    The second peak at propulsion may then extend into toe off and early swing phase and act as an accelerator of the swing leg to enable improved swing thru in the SPB gait. This may appear as increased firing action to initiate and facillitate swing phase but was sactually a secondary, but fortunate, effect left over from stance phase.

    In this way it would be reasonable to assume that it is the character of change in force impulse and HAT CoM in mid stance phase that induces increased IP action when compared to standard reference gait.

    It may also be reasonable to assume that this increased tensional force in the IlioPsoas will tend to cause a scoliosis effect in the lumbar spine and may lead to pathology and pain.

    I find this a more acceptable scenario than the scenario where the Iliopsoas fires to increase swing thru action in the shorter apropulsive gait of SPB since this would imply that the slower the CoM velocity the higher the IP force and so plotted on a graph would result in iliopsaos tensional force aproaching infinity as CoM velocity approaches zero. Clearly this would be unreasonable to assume.

    Here's some sketches to illustrate some of my points, the figures are only to highlight relative difference of forces for the sake of this discussion.


    [​IMG]


    How does this theory sit with you Howard? or anyone else that cares to comment.

    All the best Dave
     
    Last edited: Feb 12, 2009
  7. Bruce Williams

    Bruce Williams Well-Known Member

    Dave;
    I greatly appreciate your theory. I have been utilizing your CoM explanations in my dealings with patients adn practitioners and it has been helping both to understand better what is going on.
    I think that both of your above theories are overlapped more so than seperate as you propose. I postulate that Howard will tell you that as hip extension decreases and as you say the CoM velocity approaches zero that the IP tension and need to fire will indeed increase. I appreciate your idea on scoliotic changes inthe lumbar spine and also the hip rotation position, good picture to help me see what is really happening in that area.
    Nice job, now go get a life and quit doodling! :drinks
    Bruce
     

  8. Dave:

    You are assuming in your discussion, along with the sagittal plane theorists, that a "sagittal plane block" actually exists. I don't think there is any research evidence that the center of mass of the body is decelerated in its progression forward with either a "lack of ankle joint dorsiflexion" or by functional hallux limitus. This is a theoretical assumption that, to my knowledge, has never been shown by any scientific research to be an actual occurence.

    Just because we see a slowing or reversal of the forward progression of the center of pressure from an F-scan pressure insole, a pressure mat or a force plate in an individual during walking doesn't also mean that the CoM has decelerated or reversed. This idea which has been taught for many years and seems to be accepted as fact seems, to me, to be pure theory with no scientific evidence to support it. I think these center of pressure forward progression velocity alterations can be explained much more clearly using alternate theories.:drinks
     
  9. Atlas

    Atlas Well-Known Member


    For some reason(s) already mentioned and one more that I will, this research and probable current/future research is not worth the paper its written on.

    For goodness sake, there are a number of different types of LBP. Some will actually be alleviated by walking; others will be exacerbated by it. Some backs will be exacerbated by sitting; others will be helped by slouching. Some backs will have a pathological flexion limitation; some extension; some side-bending. Some back pain will manifest whilst sneezing/coughing...some will attain relief with compressive bracing and others won't; some will involve neuromeningeal structures and others wont...and the list goes on and on.

    Us pods tend to think of the lower back as one unit. It's not. With the physio hat on, a LBP presentation will have me thinking what tissue is affected(facets, discs, active tissue, passive tissue); should we loosen/de-stiffen or protect etc...



    My guess is that even if it is a factor, it is negligible. Its not the big picture.

    Don't worry about a lit review because the research is likely to be flawed (for reasons Howard has mentioned etc...)

    If you want to work out a connection, place a modified shank in footwear to reduce 1st MPJ dorsi-flexion in one sample; and compare LBP changes with the control group. That is a clinician trying to think academic:wacko:



    BTW, I like Howard's analogy of a wind-up throw and terminal stance.



    Ron
    Physiotherapist (Masters) & Podiatrist
     
  10. David Smith

    David Smith Well-Known Member

    Kevin

    I appreciate what your saying and my argument uses many gross assumptions the biggest being that saggital plane block exists. In my experiments with force plate and Vicon 3D video I have seen this pattern of gait in terms of horizontal and vertical GRF. I have not made any inductive connection or correlation with equinus ankle or FncHL. However my own gait on the right leg shows this pattern and I do tend to suffer ankle equinus on that side and here I see a double propulsion peak.

    In my clinic when I compare vertical force output pre and post ankle mobs, I very often seen a definite positive change (change for the better) in vertical GRF characteristics that could be interpreted as a change in CoM velocity characteristics.

    Clearly CoM velocity fluctuates between braking and propulsion even in the most ideal gait. I guess you would not argue that increased ankle dorsiflexion stiffness, perhaps due to tight achilles tendon will increase GRF at the forefoot and increases internal ankle plantarflexion moments due to increased achilles tendon tension. This action will also produce an angular acceleration of the CoM opposite to that of the CoM angular velocity. Therefore increased ankle dorsiflexion stiffness will result in reduced horizontal velocity of the CoM. Is there any disagreement here?

    The major assumption that links FncHL to changes in CoM velocity might be that there is a compensatory action at the STJ I.E. pronation to allow less deceleration of the horizontal CoM velocity, which leads to FncHL that then reduces the capabiltiy of the windlass action and so further reduces CoM velocity. (Or vice versa of course) As far as I know this correlation has not been shown to be probable. However it does seem to be a useful model but as you say it cannot be taken as proof.

    I will look to see if there are any studies that look for correlation between ankle dorsiflexion stiffness and CoM velocity changes. I'll get back to you then.

    As far as so called CoM progression or centre of pressure progression as characterised by F Scan or pressure mat is concerned I would agree that there is lots of room for alternative interpretation of data and one simple explaination for reversal of the CoP line would be braking starting with forefoot strike and not heel strike.

    All the best Dave Smith
     
    Last edited: Feb 13, 2009
  11. Graham

    Graham RIP

    Kevin,

    David wrote:

    At least David, Bruce, Howard et al are actually testing their thaoretical application on measurable gait parameters.

    I doubt any of us will agree on the theory but please stop calling the kettle black with regard to sagittal theory vs Kirby world. Show us what your devices do with the instrauments availble and then lets have a sensible discussion on the possible reasons.

    regards
     
  12. Dave:

    I don't think that you can assume that just because there is increased ankle joint dorsiflexion stiffness that a reduction in horizontal velocity of the CoM will also occur in late midstance/propulsion. My belief is that the central nervous system will always try to conserve horizontal momentum of the CoM and keep the CoM horizontal velocity as constant possible in level walking. Conserving momentum of the CoM of the body is the animal's method of preserving the economy of locomotion. Economoy of locomotion is one of the prime driving forces behind the function of the central nervous system during locomotor activities in most, if not all, animal species.

    Increased ankle joint stiffness doesn't cause a "sagittal plane blockage", but rather results in either an earlier heel off and/or increased dorsiflexion of the forefoot on the rearfoot and/or a more abducted gait pattern and/or a shorter stride length, depending on the relative dorsiflexion stiffness of the forefoot on the rearfoot, ankle joint dorsiflexion stiffness and many more mechanical variables that may or may not be under the control of the central nervous system.

    All I am saying here is that this idea of "sagittal plane blockage" has never sat well with me given my knowledge of the biomechanics of the human foot and lower extremity and of the physiology and biomechanics of animal locomotion. Do alterations in CoP progression/velocity/position occur with different alterations in foot anatomy and joint function? Yes. However are these alterations in CoP progression/velocity/position an indication of CoM deceleration due to a due to "sagittal plane blockage"? I doubt it.
     
  13. Graham:

    Speaking of black kettles.....please provide me a list of the research papers that you have authored or coauthored that support your sagittal plane theories or your treatment results. I am actively involved in research on my theories and have coauthored papers recently on my theories and will soon have my third book describing my theories and my treatment results. The question is, what have you done lately, or ever, in this regard, Graham??
     
  14. Graham:

    Speaking of black kettles.....please provide me a list of the research papers that you have authored or coauthored that support your sagittal plane theories or your treatment results. I am actively involved in research on my theories and have coauthored papers recently on my theories and will soon have my third book describing my theories and my treatment results. The question is, what have you done lately, or ever, in this regard, Graham??:drinks
     
  15. David Smith

    David Smith Well-Known Member

    Kevin

    You wrote
    I do feel that SPB and change in CoM velocity does exist as a reaction to equinus and FncHL however I am surprised to find that I cannot find any papers that investigate, as an experiment, the probability of that correlation let alone indicate a causation. There are some or even many that would lead to some deductive reasoning as to the possibility of this action. (I have attached some examples) There are many discussion papers that make this assumption but none that I can find that actually investigate this precisely. This is surprising since it would appear on the face value to be a simple experiment.

    Therefore your comments are correct and further research is required to validate assumptions made by many including me. For now however I will continue to use saggital plane theory as a guide to biomechanical evaluation and patient treatment since it appears, amongst several others I casually warble, to be quite a successful convention


    Cheers and all the best Dave Smith
     
    Last edited: Feb 13, 2009
  16. David Smith

    David Smith Well-Known Member

    Here's the attachment I hope since it didn't attach to the last post for some reason.
     
  17. Dave:

    I will need to disagree with you here. What is being called "sagittal plane blockage", I believe, is not a true "blockage" of sagittal plane motion but is more a gait compensation for a increased stiffness at a joint. In addition, these increases in joint stiffness don't necessarily imply that the center of mass (CoM) is decelerated by these gait events. I believe that, instead, the CoM is not decelerated by these events and the CoM horizontal velocity is relatively constant even as these alterations in joint stiffness occur or what you and the sagittal plane theorists call "sagittal plane blockages".

    As far as measuring CoM movement/velocity being a "simple experiment", I don't think it would be that simple. Determining center of mass is not an easy task during gait since the head, trunk, upper and lower extremity 3D positions, and their respective masses must all be taken into account. One would need 3D gait analysis on all the body segments, and their masses to get a fairly good idea of where the CoM is at any point in time. Simple walking speed and pelvic movement does not necessarily accurately reflect actual CoM speed or movement.

    As far as treatment using sagittal plane theory, I really have no problems with it since I treat patients with orthoses in a similar fashion to the way that Howard, Bruce and Graham treat their patients. However, our theoretical explanations as to why the orthoses give therapeutic results often varies quite widely. In fact, Graham and I once lectured together in a gait examination clinic and found that we actually were making similar orthosis adjustments to patients, but were using totally separate theoretical explanations as to why we made those orthosis adjustments.

    If we all agreed with each other, there would be nothing to discuss!:drinks
     
  18. David Smith

    David Smith Well-Known Member

    Kevin
    Very true.

    When you say that compensations will allow the velocity of CoM to remain constant do you mean that the Mean or average velocity will remain constant over time or that the variation in velocity amplitude and frequency will remain constant over time.

    I.E. Since, I feel, we can be fairly certain that there is a sine wave variation in CoM velocity during gait progression, do you feel this will remain insignificantly altered where there are adaption or compensation to anatomical and biomechanical variation?

    If there were a significant change in sine wave amplitude or frequency then I am sure there would be significant accelerations of the COM, particularly the HAT CoM,that would alter muscular actions in response to those new inertial forces.

    Simple experiments eh! is there such a beast when it involves live beasts.

    I had my head checked
    by a jumbo jet
    it wasn't easy
    it never is is.

    Who sung that? Simon will know. SIMON!!


    Got to go to Brazilian Jiu Jitsu now, speak again soon.

    Great discussion

    Dave :drinks
     
  19. Dave:

    Why would an early heel off necessary increase the CoM velocity? In order to make that assumption, one must know the direction and magnitudes of the ground reaction force (GRF) vector relative to the center of mass (CoM) for both the normal heel off condition and early heel off conditions and, also, the contralateral limb must be in swing phase. Just because the heel lifts off early, does this also necessarily mean there is a greater posteriorly-directed horizontal shearing force from the foot on the ground? I don't think so. In fact, the early heel off is more likely to cause a change in the path, but not the speed of the CoM, as the CoM raises earlier in stance phase versus the normal heel off condition.

    I am attaching some drawings from my new book (Kirby KA: Foot and Lower Extremity Biomechanics III: Precision Intricast Newsletters, 2002-2008. Precision Intricast, Inc., Payson, AZ, 2009) that I have the final proof of, sitting on my desk this morning, ready for printing. In the drawing, I have illustrated three types of feet going through three different phases of progression of the CoM over the foot. All three feet have different spring stiffnesses in the midtarsal-midfoot joint and the one with with a high stiffness has, what you and the sagittal plane theorists call, a foot that has "sagittal plane blockage", since the ankle does not dorsiflex normally relative to the tibia. You can see, that with the stiffer spring, the earlier heel off occurs and with a more compliant spring, a later heel off occurs. In addition, in the foot with a stiffer midtarsal-midfoot spring, the hallux will dorsiflex normally and with a more compliant midtarsal-midfoot spring, the hallux will tend to have restricted dorsiflexion due to functional hallux limitus.

    This, in my opinion, is not and should not be called "sagittal plane blockage". This is, rather, an interindividual variation in the spring stiffness of the ankle-STJ-MTJ-midfoot complex that causes the central nervous system to determine the optimum method by which they can allow their CoM to progress over their foot and lower extremity with it's given load-deformation characteristics, with as constant of a CoM velocity as possible to optimize gait economy.
     

    Attached Files:

    Last edited: Feb 14, 2009
  20. David Smith

    David Smith Well-Known Member

    Kevin

    You misundersatnd me, I said it would change the velocity due to an acceleration induced by an additional horizontal force. This can equal a reduction or increase in velocity.

    Thank you for your diagrams, which for convenience show GRF as vertical and has no horizontal component. In reality if the GRF is not directly below the CoM then there must be a horizontal componet, which will induce a horizontal acceleration, an acceleration is a change in velocity vis a vis the CoM will experience a change in velocity that will neccessitate and muscular reaction.

    Cheers Dave
     
  21. Blur: song 2 (tune! BTW)
     
  22. Dave:

    I don't think that just because there is a horizontal shearing force directed posteriorly from the foot on the ground that the center of mass (CoM) is accelerating. It would seem, due to the inertial properties of the body, that the the CoM could also be remaining at constant velocity or the CoM could be decelerating when a there is a horizontal shearing force directed posteriorly from the foot on the ground. However, I would agree that an increase in horizontal shearing force directed posteriorly from the foot on the ground, while the contralateral foot is in swing phase, will tend to accelerate the CoM forward.

    My diagrams did just show a vertical ground reaction force vector to try and illustrate a point. However, you are right in that the ground reaction force vector would continually change in spatial orientation to the foot as the CoM moved over the foot during stance phase.
     
  23. Graham

    Graham RIP

    Kevin,

    I didn't think this was an arena for researchers only! After 12 years in the profession I did a further Hons degree in Pod Med in 1997 through Brighton University Podiatry Dept. I looked at the evidence behind "conventional" biomechanical wisdom (0) and demonstrated that the gait parameters that Howard said he was looking at and could "improve" could be looked at and "changed".

    Not all of us have the resources to undertake research. All of us have the ability to become Critical thinkers.

    There is a big diference in wanting to understand the effect of our foot orthoses using objective based assessment techniques and selecting research projects aimed at proving one's own theories!

    I understand now why Howard is a rare contributer to this forum.

    Kevin, It is unlikely I will ever have the ability or resources to undertake dynamic effect research. I will however always be critical of the broad based assumptions made when viewing the biologically variable body, and it's individual interaction with an artificial world, in a strict structural engineering enviroment.

    Not withstanding. Your "ideas" are thoughtful, provocative and enlightening.

    Regards

    Graham
     

  24. Graham:

    Good research that validates sagittal plane theory simply doesn't exist and research by VanGheluwe et al seems to refute the theory (Van Gheluwe B, Dananberg HJ, Hagman F, Vanstaen K: Effects of hallux limitus on plantar foot pressure and foot kinematics during walking. JAPMA, 96:428-436, 2006). Therefore, when you start talking about theories not having proof, I was always taught that people in glass houses probably shouldn't be throwing stones.

    When you can provide me with research that shows, for example, that functional hallux limitus causes arch flattening or that the swing leg somehow pulls the body forward, then I will be much more eager to jump on the sagittal plane theory bandwagon. Until then, I will try to stick to using Newtonian physics to support my theories.

    Podiatry Arena is a great place to discuss theory, there is no other like it. However, when you start attacking theories that I have been working on for nearly half my lifetime, then don't expect me to throw out the red carpet for you.:drinks
     
  25. Graham

    Graham RIP

    Kevin,

    And when you continue to attack theories that others have been working on for just as long, but don't fit your thinking, don't expect us all to roll over and accept blindly what YOU believe.

    Regards,
     

  26. Graham:

    Contrary to what you may think, I actually like it when others don't "roll over and accept blindly" what I believe. For these people, I have great respect, like I have for you.

    I greatly enjoy discussing things here on Podiatry Arena with the members who can challenge my ideas with new research, better physics knowledge, better biomechanics knowledge, better physiology knowledge, etc. I can learn more from these individuals. I like to learn new things. But I also don't mind speaking up when others make statements that don't either conform to Newtonian physics, don't conform to accepted biomechanical principles, don't conform to accepted physiology knowledge, and don't conform to my clinical observations.

    As I said earlier to David Smith, if we all agreed on everything here on Podiatry Arena, there would be nothing to discuss.:drinks
     
  27. Dananberg

    Dananberg Active Member

    Kevin,

    I do not believe I have ever said that the CoM is decelerated by sagittal plane restrictions. In fact...its the opposite. It is the motion of the CoM that drives the entire system. This is why sagittal plane restriction is so compelling. The force that is present to move the entire body forward is due to a complex interaction between muscle function and energy storage/return mechanics. The ability to conserve momentum plays a highly significant role, as it is all designed to move the CoM over the foot.

    Therefore, as the CoM moves forward, but the foot/ankle fails to permit it, there is an ever present need to either store or dissipate this energy. Considering that pathologic pronation occurs in the 2nd half of single support phase, and this is the time when the CoM is undergoing max acceleration, then the correlation between the two would seen hard to ignore. The late phase pronation we see is as much related to the sagittal plane motion restrictions and subsequent requirement to dissipate these forces. I would agree that the restriction may be due to many factors, including but certainly not limited to STJ axis deviation. Finding what and why these exists becomes the art of biomechanical therapy, keeeping in mind that the CoM is already in motion....letting that translate to the floor is the treatment goal.

    As far as your diagrams are concerned, there is one issue I would like to discuss. The increase in GRF shown under the met heads is incorrect in the first case. The vertical pressure loads increase when the entire metatarsal rotates thru the sagittal plane until it comes as close as possible to vertical. While shear forces may increase in the case you demonstrate, the vertical load does not. Vertical load is related to sagittal plane orientation. The less sagittal plane movement, the less vertical load sub met heads.

    Howard
     
  28. efuller

    efuller MVP

    Howard, We have had this discussion before and I still disagree. The vertical is not related to the angle of the met heads. Here's a simple thought experiment. Stand and just lift your heel off of the ground. The angle of the metatarsal heads is close to that with the heel on the ground. With the heel off of the ground the veritcal load is body weight. Now raise up by maximally plantar flexing the ankle. In this static position, the weight on the metatarsal heads is body weight. The same amount of force will be distributed across the metatarsal heads regardless of the angle of the metatarsal heads to the ground. There will be a much larger bending moment on the metatarsals when the heel is just off of the ground.

    Regards,

    Eric
     
  29. Dananberg

    Dananberg Active Member

    Eric,

    You're right...but only in that we have gone round and round about this. You are wrong about vertical load transfer. Chapter 2 in Root's text is very clear about this concept.

    I just stood on one of my F-scan sensors. With my heel off the ground, but just barely, the load on my forefoot was minimal. (I could also feel the tension in the arch.) The further my heel was lifted (and the more my met heads rotated sagittally to permit this), the greater the forefoot load (and the less arch tension). The more I lowered my heel (but did not touch it to the floor), the less metatarsal load. Since my weight did not change during this trial (I wasn't eating), and my position did not change (I wasn't walking), the only change was the angle at which my metatarsals were inclined to the support surface. This led to a change in vertical load under my met heads.

    When observing patient's gait with F-scan, the changes in the force/time curves are related to the changes in position of both the CoM and foot. As the CoM advances, but the foot not change its position (ie, failure of the sagittal plane to change) , the load mix changes just as in my experiment above, with less vertical and more tensile load (born by the soft tissue..ie increased arch tension) being present. The more the CoM moves forward, and the less the foot moves, the greater the difference and the more soft tissue stress develops.

    How you choose to correct this should be the discussion. The way the foot manages weight transfer is fairly straight forward.

    Howard
     
  30. gush_horn

    gush_horn Member

    sorry to digress but can someone define CoM?
     
  31. dyfoot

    dyfoot Active Member

    Hi,

    I think that would be centre of motion.

    Although if not moving, it would be centre of gravity.

    Cheers Brad:drinks
     
  32. efuller

    efuller MVP

    Center of mass. Essentially the average point of mass. When standing it's somewhere in the middle of your belly. If you did the yoga pose of downward facing dog, your center of mass would be somewhere outside of your body. between your belly button and the ground.

    Regards,
    Eric
     
  33. Atlas

    Atlas Well-Known Member

    This thread was about the relationship about 1st MPJ pathology and back pain.:dizzy:


    The profession is still in a dark grey cloud.




    Ron
    Physiotherapist (Masters) & Podiatrist
     
  34. efuller

    efuller MVP

    I pulled out Root. What section in chapter 2 are you referring to. I didn't see any reference to increased vertical forces with increased inclination of the metatarsals. Besides the chapter is filled with inaccuracies in regards to physics.

    Elsewhere, I have seen something I think was called the parallelogram theory, that tries to explain this phenomenon using vectors. The problem with the theory was it did not look at the input forces. When a body is standing, and not accelerating, the total force on the foot has to equal body weight. No matter how you draw the vectors the vertical vector has to equal body weight.

    We agree your weight did not change. I stood on a scale with heel on ground and heel just off ground and ankle maximally plantarflexed. The reading of the scale did not change. So, the total force on the foot remains the same. When the heel is on the ground, the total force on the foot is divided between the heel and the forefoot. When you sum the force from all locations it will equal body weight. When the heel is off of the ground, and the body is not accelerating, then the sum of force on all of the met heads has to equal body weight. If we define load as total force (and not pressure) then it is not physically possible for there to be less than body weight on the metatarsal heads when the heel is off the ground and the body is not accelerating. If the force is not on the met heads where is it?


    This reminds me of a presentation at the EMED users conference in 1991. The EMED insole had just come out and someone thought it would be cool to see if the forces inside the shoe were different than outside of the shoe. The conclusively proved with excellent statistics that ground reaction force inside the shoe was approximately 2/3 of force outside of the shoe. Those who understood the physics realized there was a problem with the insole. It was a calibration problem that they have since solved, but the point is you should believe the physics over a readout of a machine.

    The F-Scan had a similar problem that they solve using some proprietary algorithms. In other words a fudge factor to make the total force under the foot come out to a number close to what it should. If you don't plug in a person's body weight into the F-scan the total force time curves come out screwy. Even Techscan admits that you should not use the F-scan sensors for research without doing a calibration with a bladder with known pressures.

    Even though I don't think the F-scan can necessarily provide research quality data, it can provide data that helps you modify an orthotic to improve outcomes.

    I don't see why we should limit the discussion on this academic forum. The discussion of forces is something that comes under the heading of biomechanics. Perhaps, in a different thread... Apparently the way the foot manages weight transfer is not so straight forward.

    Cheers,

    Eric
     
  35. Dananberg

    Dananberg Active Member

    Eric,

    First of all, the issues of accuracy with F-scan and E-med were in the early 90's. The technology has advanced considerably, and as far as I am aware, F-scan data has been shown to be extremely accurate, even in a research setting. If you are really interested, I can dig up the references.

    You really missed my point in this discussion (sort of like missing the forest because the trees are in the way). Weight is best managed when the osseous structures are appropriately positioned. In very planus feet, the mets are essentially parallel to the floor. The weight must therefore be borne by the soft tissues and arch pain develops. When these same mets can be maneuvered so that they align themselves more towards vertical, they bear more of the body weight and the soft tissue is under far less stress. That is the entire point, and conceptually transfers to issues with feet while walking. Move the metatarsals towards vertical (ie, sagittal plane motion), and the foot supports far better than when this does not happen.


    Howard
     

  36. As Eric stated, and as I have noted in my earlier posts on this thread, CoM refers to center of mass. Center of mass is a commonly used term within the international biomechanics community and within physics, to describe the point three-dimensional location where the overall mass of an object can be thought to be concentrated. It is very handy when we analyze the motion patterns of a complex object, like the human body, where we have a central trunk but also a moving head, arms and legs, to use the center of mass (CoM) as a way to predict how that object will move under the influence of forces such as gravity, ground reaction force, etc.

    One of the more interesting and fascinating mechanical analyses of the CoM of the body is in the motion analysis of a high jump. In the Fosbury Flop high jumping technique (i.e. head first, jumper's face looking skyward), the CoM will actually pass below the bar, rather than above it, if the technique is done correctly. This is because, during the jump, the greater sum of the mass of the body will always remain below the bar, rather than above it, therefore allowing the athlete to jump over a higher bar, than if their CoM was required to actually go above the bar.

    Hope this helps.
     
  37. Howard:

    Perhaps I misunderstood what you were trying to say in regards to the center of mass under the influence of "sagittal plane blockage". What then is your definition of "sagittal plane blockage" used in reference to sagittal plane facilitation theory? Wouldn't you think that the term "sagittal plane motion modification" would be a more accurate way to phrase this phenomenon?
     
  38. David Smith

    David Smith Well-Known Member

    Eric and Howard
    I would guess that there is some misinterpretation and talking at cross purposes going on here. As Eric correctly states, In stance there can only be a force applied to the foot by the ground equivalent to body weight regardless of the part or angle of the foot in contact with the ground. However Howard says
    and
    Howard is referring to the change in discreet force under the met heads as characterised by the F scan output where the data is masked to only include output from the met head area. Therefore as there is also data, from other parts of the foot when the heel is only just off the floor, which is not included in the output then there is a difference, i.e. change of peak force, in the masked output which is characterised in the full plantarflexed ankle position as an increase in force on the forefoot.

    The question previously put was does the CoM change velocity due to what is known as a ‘saggital plane block’? This is really a tautology since a saggital plane block infers that there is a block of forward progression that must result in a change of CoM velocity. So therefore the question arises is there such a thing as saggital plane block?

    We must agree surely that there does exist braking and propulsion thru any bipedal gait that causes a translation of the body mass from point a to point b.
    For this to be so there must be a change in CoM velocity during each full gait cycle. This can be characterised by a graph showing anterior- posterior applied ground reaction force over time. This graph shows a negative and positive force impulse. In walking, the area beneath the positive and negative curves will be equal while the average CoM velocity (walking speed) is constant e.g. while walking at 5kph (or 3mph). This must also be so otherwise the subject of interest would be slowing or increasing average walking speed i.e. accelerating.

    From this model it can be seen that to maintain an average constant velocity (walking speed) of the whole body mass the positive and negative impulses must be approximately equal if we assume frictional losses are negligible. Therefore it is the nature of the change in the curve shape that will indicate rate of changes in the velocity of the centre of mass during one gait cycle.

    Since force x time = impulse and change in momentum = mass x change in velocity => force x time then a change in impulse must result in a change in momentum. Since mass remains constant and momentum = mass x velocity then there must be a change in velocity.

    Would you agree that if we compare a subject that walked slowly with very long strides (slow cadence) to one that walked at the same speed but with short steps (fast cadence) the impulse curves and areas would be entirely different.

    I would guess that the former would experience higher braking and so would have greater force impulse amplitude and magnitude, greater area and the slope change from braking to propulsion and crossing zero would be much steeper because he would also be required to accelerate to compensate for the loss of momentum at braking.
    Could the former gait style be referred to as a saggital plane block?

    I would guess that you would answer No, since there is no pathological block and the average constant velocity (walking speed) remains the same. However there is a large change in the rate of change of velocity i.e. accelerations, occurring thru each gait cycle.

    The two subjects of interest maintain the same walking speed because they adapt or compensate in some way to allow them not to slow down or reduce average velocity.
    Is it not possible then that, if just changing the step cadence for a given walking speed changes the impulse curves, any biomechanical / anatomical variation might change braking and propulsion force impulse characteristics and therefore change the momentum and so velocity of the CoM?

    If this is true then to recover momentum after excessive braking and return a constant walking speed the body must make some compensation that accelerates the CoM. This can only be achieved by some additional muscular action. Could this not then induce a force impulse in the muscle that was pathological over time.

    I would suggest then that saggital plane block while being a useful description of a biomechanical variation is not an entity of itself but rather a point on a scale where the force impulses induced by a certain gait style becomes pathological. Like most biomechanical variations there is no absolute measure of where impulse magnitude equals pathology only the magnitude that causes pathology for a certain subject of interest.

    Therefore it would not perhaps be unreasonable to argue that saggital plane does not exist in terms of entity but in terms of cause and effect it is possible to argue that it does exists since if an effect exists then just as equally so must the cause.

    Just some thoughts to mull over

    Cheers Dave
     
    Last edited: Feb 21, 2009
  39. David:

    After reading these last two paragraphs.....have you ever thought of a career in politics?......we could use some good ones here in Sacramento now since it took our politicians in the state capitol of California over 3 months after the budget deadline to approve a budget!:wacko:

    All kidding aside, I think we first need a good definition of "sagittal plane block" if we are to progress any further in this discussion. I asked Howard this question this AM and maybe he will give us a good definition to work with so that we can have an intelligent discussion on whether it exists or not. In addition, maybe the term simply needs to be renamed or eliminated to reflect the biomechanics of what is actually happening in the foot, lower extremity and rest of the body with entities such as equinus deformity and functional hallux limitus, which Howard claims creates "sagittal plane block".

    I suggest that a term such as "gait alteration due to increased dorsiflexion stiffness" (GAIDS) would be a more appropriate term to reflect our current knowledge of how alterations in the load-deformation characteristics of the joints of the ankle and/or foot may affect the kinematics and kinetics of walking gait.
     
    Last edited: Feb 21, 2009
  40. David Smith

    David Smith Well-Known Member

    Kevin

    Oh yeah! a few years in California earning loads for not doing much, sounds good to me. Can I be a film star too? I'll be back, asta la vista baby, don't push me, you talkin to me! you talkin to me! see I know all the hooks and I'm strong.

    Cheers Dave

    BTW the acronym GAIDS is also associated with General Agency Development Insurance Service, - Generalised Almost Ideal Demand System (could apply here quite well) and Gay AIDS, (http://uncyclopedia.wikia.com/wiki/GAIDS), which is far to un-PC for a politician. :)
     
    Last edited: Feb 21, 2009
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