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Measures for Identifying changes in 1st ray dorsiflexion stiffness in terms of discreet plantar pres

Discussion in 'Biomechanics, Sports and Foot orthoses' started by David Smith, Nov 25, 2009.

  1. David Smith

    David Smith Well-Known Member


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    Measures for Identifying changes in 1st MPJ dorsiflexion stiffness in terms of discreet plantar pressures/forces

    Martin

    You wrote


    My thesis indicated that there is no increase in plantar fascia (PF) strain during the stance phase time from Heel Contact (HC) to Hallux toe contact (TC). There is an increase in the length and corresponding decrease in the height of the medial longitudinal arch (MLA) during this period, which is allowed by the unwinding of the windlass as the hallux dorsiflexes to the ground.

    The toe contact (TC) was at 33% of full stance phase, (At 39% stance the hallux was at full plantarflexion in terms of kinematics0 - 100% stance = 850ms, the heel off (HO) was at 57% stance and between these to markers there was a small lengthening (and lowering) of the MLA which did increase PF stress and strain. However most of the PF strain occurred after HO at 57% stance and peak strain occured at 83% (705ms) stance which also directly correlated with peak sub hallux pressure. Peak sub 1st MPJ pressure occurred at 75% stance, peak propulsive phase GRF occurred at 704ms.

    It was formally established that the foot posture and gait parameters used in the experiment was normal by all published standards, kinetic and kinematic, it was assumed that the results indicated that the function was normal and did not suffer FncHL in clinical terms. This was backed up by visual evaluation.

    It was concluded that FncHL would occur when the MLA lengthened (lowered) excessively during the period 33% to 57% stance or between TC and HO. This would result in increased stress in the PF and so, thru the windlass action, increased Sub hallux GRF.

    Therefore in the situation where there was no clinically evident FncHL the peak vertical force sub 1st MPJ should occur before the Peak vertical force sub hallux. It was extrapolated from the data that when FncHL existed that sub 1st MPJ force would peak after the sub hallux peak force. This proposal would require further investigation to substantiate.


    The term excessive in terms of MLA lengthening (lowering) from TC to HO would also need further investigation to clarify and define in quantitative terms. However PF extension in this period was only 1.2mm in a total of 4.5mm strain for the full PF length at full stress. The time from TC to max hallux plantarflexion (33%-39%) in stance may account for most of this, i.e. as the plantar hallux soft tissue compresses under load. It may be that there is a minimum ratio here between total strain and strain in the TC-HO period e.g. in this case 3.75:1. It might also be reasonable to say that for optimum performance / efficiency the MLA should not lengthen (lower) after maximum hallux dorsiflexion in stance.

    It is interesting to note that it was found that in the period from HO to peak PF strain and sub hallux vertical force at 83% stance, the MLA shortened as the hallux dorsiflexed, however the displacement due to hallux dorsiflexion about the windlass capstan was greater than the shortening / negative displacement of the MLA. This retarding of the MLA shortening may also be significant.

    Martin - Is this the sort of data you were thinking of to use to build into an outcome measure in terms of FncHL improvement?
     
    Last edited: Nov 25, 2009
  2. Mart

    Mart Well-Known Member

    Re: Measures for Identifying changes in 1st MPJ dorsiflexion stiffness in terms of discreet plantar pressures/forces

    Hi David

    Great summary and yes exactly.

    My thought was to use your idea (perhaps others have described this too, I am not sure) regarding the measure quoted above and test it against another index for consistency.

    It is appealing to me as a measure because;

    it seems plausible based on our current understanding of the windlass mechanism,

    it is easy to test if in-shoe (or barefoot) pressure measurement studies are being conducted for any reason ( I routinely do 4 or so per week for a variety of reasons)

    it has capacity to test foot orthoses for efficacy other than pain VAS or kinematic measures

    and as far as I am able to understand may be free of confounding variables associated with calibration or system type since it is may be made dimensionless and doesn't depend on calibration accuracy since it is temporal.

    IPP (instant to peak pressure) and IPF (instant of peak force) data is automatically extracted in Tekscan Research v 6.31 and later and I suspect most other systems.

    If expressed as a ratio of timing from HC as the plantar digital area 1st toe/1st metatarsal head , either as absolute time or proportion of contact phase regardless then

    FncHL would be defined as present if

    ratio is 1 or more

    absent if < 1


    The excel SS I posted a couple of weeks ago automatically calculates this from anatomically templated regionally extracted data and flags if test +ve.

    To make this meaningful (or futile), what I think needs fleshing out is what this might be usefully compared to and what might confound this approach.

    So far I have compared these values to what I do as a simple clinical test to evaluate what I believe is a useful measure of predicting if gait compensation is required to deal with FncHL.

    This test (which I understand common place), involves non weight-bearing passive max dorsiflexion of 1st ray at MCJ (with plantar metatarsal head thumb force) and whilst maintaining this, passive dorsiflexion of hallux at metatarso-phalangeal joint (force plantar to distal phalanx). If there is much increased resistance or locking this is compared to passive plantarflexion of 1st ray. Currently, I regard this as my index of FncHL (criticism encouraged) if MCJ dorsiflexion locks and plantarflexion unlocks metatarso-phalangeal joint dorsiflexion.

    To date all but one ratios flagged for +ve test also were +ve for clinical manipulation test. But many with manipulation test +ve are -ve for ratio test.

    There are a multitude of explanations to explain this but perhaps a good starting point for constructive brainstorming around issues is to consider a few.

    So to kick off; how do others test for FncHL, perhaps this has already be flogged to death? I think my technique mimics that taught by Craig Payne?

    Is FncHL mostly perceived purely function of 1st ray dorsiflexion stiffness or other stuff (perhaps also flogged to death elsewhere on forum)?

    My understanding is that Kevin Kirby has made a good case (I understand you did too) that, based on interpretation the equilibrium of joint moments at any given instant, 1st ray stiffness (at TNJ) takes precedence as most influential variable in behaviour of 1st metatarso-phalangeal joint towards ens of midstance not withstanding presence of hallux limitus. It seems to me there is likely a continuum between dorsal metatarso-phalangeal joint osteophytosis ie hallux limitus causing 1st metatarso-phalangeal joint stiffness and FncHL (purely in terms of 1st ray stiffness). If so should they be distinguished given that they are not mutually exclusive and if so how or even why?

    Mechanically, from a therapeutic point of view, initially I mostly treat them (HL and FncHL) the same way (by attempting to reduce 1st metatarsal head ground reaction force during mid stance).

    I saw the first case this week (which I will find some time to prepare brief case study over weekend) with obvious asymmetric kinematic and kinetic consistency with your notion of FncHL as a timing and 1st ray stiffness issue but complete lack of clinical signs using passive motion I described.

    I think this may be a key (of a bunch) to understanding but goes against the grain (probably because I have some false premises).



    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
     
  3. David Smith

    David Smith Well-Known Member

    Mart

    Where was this posted?

    dave
     
  4. David Smith

    David Smith Well-Known Member

    Re: Measures for Identifying changes in 1st MPJ dorsiflexion stiffness in terms of discreet plantar pressures/forces

    Martin

    1) First off let me say I believe that the term Functional Hallux limitus is a useful but arbitrary one. It is a term that allows easy communication of a complex mechanical function in clinical terms to express the concept of a certain point where an undesirable action takes place that negatively affects gait progression.

    To steal a term from Kevin Kirby the 'increased dorsiflexion stiffness' or rather 'change in d.flex stiffness' of the 1st MPJ to GRF is progressive in nature through the stance phase of gait. Not only the magnitude of maximum stiffness but also the time of maximum stiffness is important to consider.

    The magnitude of dorsiflexion stiffness may not be important in absolute terms and may be relative to body weight and limb length i.e. a normalised value would be more useful.

    A certain stiffness of the hallux to dorsiflexion by GRF is desirable, however there will be a magnitude that causes a compensatory action to take place to avoid slowing the CoM progression significantly. This can be called a perturbation of saggital plane progression, both the cause and effect or increased stiffness and compensation can be classified as a perturbation in the gait progression.
    It may be there is a normalised value of d/flex stiffness that tends to cause a perturbation.

    At this point there is a major hurdle; How do we define if the increased d/flex stiffness of the 1st MPJ (FncHL) is the cause of a perturbation or the effect of a entirely different and unrelated perturbation.

    This not withstanding it would be convenient if we could define that normalised value and then identify it in the clinical situation.
    2) If I understand your test proposal; You will compare the point of significantly increased d/flex stiffness in the passive non w/b situation to the w/b situation in the same kinematic conditions.

    This brings up 2 or 3 questions; At what point of 1st ray dorsiflexion will you test hallux d/flexion stiffness? How will you know if the force applied to the hallux is significant in terms of gait progression perturbation? Can you expect to get similar kinetic conditions N/w/b to w/b in terms of internal v's external forces?

    This next point is an obvious but important consideration.

    The Plantar fascia is thin at the 1st MPJ where it wraps around the windlass capstan when compared to the origin and the main body of the PF.
    This means that for any given load the stress at the thin end is much greater therefore so is the strain. This is convenient since this allows the hallux to dorsiflex about the the met head without corresponding shortening (raising) of the MLA being necessary. This happens (in my experiment) after HO to peak sub hallux pressure in the normal windlass operation i.e. the PF is increasing in length as the MLA shortens. This elasticity of the thin end equated to about 12dgs of hallux dorsiflexion while still remaining in reasonable safe working load tolerances. Therefore if the MLA is excessively lowered (within certain limits) the hallux will still be able to dorsiflex by utilising this elastic property of the PF, perhaps as much as 20dgs before the hallux d/flex stiffness is reaching the critical normalised value mentioned earlier.

    So if the MLA is excessively extended between HC and HO then the tension in the distal PF may already be approaching the magnitude that causes hallux dorsiflexion stiffness to be at the critical normalised value. At this point there may be a compensation to avoid perturbation but equally there may be a compensation to avoid tensile stress trauma to the PF. By my calculations in my thesis the Ultimate tensile strength of the PF is twice that of the normal operating stress and the elastic limit is 30% below it maximum limit. If the stress loads were to approach those limits then an antalgic or injury aversion response may occur.

    All these characteristics come under the term FncHL but would need further investigation to define what they mean in terms of progression perturbation.

    As you might also be saying, it might be feasible to look a the relative discreet plantar pressure timing and magnitudes between certain events of stance. Then compare these to obseved indications of FncHL, however I don't know about others but determining if FncHL is definentely present can be difficult by visual evaluation alone. I tend to assume FncHL by the compensations observed and the biometrics measured. This however returns us back to the major hurdle mentioned earlier - chicken or egg :confused:

    I think we need first to define in a more robust manner what and when exactly it is that FncHL occurs.

    That's enough for now, I'll let you chew that bit over for now. Good discussion Mart :drinks

    Dave
     
  5. Mart

    Mart Well-Known Member


    If you go to my web site - navigate to resourses page and click on podarena icon it should allow you opotion to download the file

    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
     
  6. Mart

    Mart Well-Known Member

    David smith said
    “As you might also be saying, it might be feasible to look a the relative discreet plantar pressure timing and magnitudes between certain events of stance. Then compare these to obseved indications of FncHL, however I don't know about others but determining if FncHL is definentely present can be difficult by visual evaluation alone. I tend to assume FncHL by the compensations observed and the biometrics measured. This however returns us back to the major hurdle mentioned earlier - chicken or egg

    I think we need first to define in a more robust manner what and when exactly it is that FncHL occurs”.

    Hi David

    Again a great summary and you mentioned some stuff regarding distal compliant end of plantar fascia which I had forgotten about. Also your points regarding defining the terms more precisely; I completely agree and your concerns and I think concisely consider the problems with terminology and why it may be impossible to progress further with this idea without redefinition. I recollect that Craig Payne has attempted to classify metatarso-phalangeal joint dorsiflexion stiffness by qualitatively dividing passive “pre loading” of hallux in to 2 approximate position something like early and late windlass operation. If I understand the intent of this it was along the same line in attempting some classification.

    One of the issues I find hard to be clear about is interpreting when “gait compensations” are attributed to avoiding 1st metatarsal head ground reaction forces in attempt to improve the perturbations which you talk about (and I think underpin what Dannenberg was attempting to achieve) and when, as you know there are more plausible explanations (and I think what Dannenberg’s work misses).

    How about this for a bunch of assumptions towards building an argument to progress the idea;

    IF

    gait compensations (which need defining in terms of kinematics and kinetic more robustly than Dannenberg) for this “theoretic mechanical problem” of equilibrium of joint moments and 1st ray position (lets continue using FncHL for time being)

    ARE

    Cause of compensation (as opposed to some other phenomena)

    THEN

    if it is true that there is “useful” foot orthoses intervention

    THEN

    we ideally should be able to detect some evidence of associated change.

    NOW

    to make useful investigation of effect of foot orthoses in-shoe pressure measurement studies are need

    BECAUSE

    kinetic measures pertaining to the foot are invisible (inside shoe) and difficult to measure (large error in small distances)
    in-shoe pressure measurement studies probably are only option clinically (and probably in research).

    Give me a bit of time over weekend to post some interpretation of the asymmetric case I mentioned earlier because I think it might be usefully illustrative and reveal some reasoning flaws ect.

    Great to flesh this out . . . I have wanted to do this for a while.

    Good to see you still passionate about this Graham too. Do you fancy posting the research you did on this a few years ago when you were working at the Ottawa Rehab Center, I seem to remember reading the brief report you did with Lemaire regarding some in-shoe pressure measurement studies on this subject???? not sure if it was ever published,


    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
     
  7. David Smith

    David Smith Well-Known Member

    Martin

    You wrote
    Like you Mart I will have to take some time to consider this stuff.

    Cheers Dave
     
  8. Mart

    Mart Well-Known Member

    Definitely; sometimes the best we can do is see that something is unlikely or better still impossible, but that is progress

    Interesting comment from the prof, I love those humbling wake up calls:empathy:

    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
     
  9. Martin and Dave:

    Interesting discussion. I just had time this morning to read through it all and wanted to add a few points.

    I believe that the term "functional hallux limitus" (FnHL) is a good clinical term since it helps us separate out "structural hallux limitus", where there is a reduced range of hallux dorsiflexion in the non-weightbearing setting, from FnHL, where there is reduced hallux dorsiflexion only in the weightbearing setting.

    In order to best describe the mechanics of FnHL, and why it occurs in some feet and does not occur in other feet, we must understand the complex interactions of many joints including the ankle joint, subtalar joint, midtarsal joint, midfoot joints, first ray and first metatarsophalangeal joint (MPJ). In addition, if we are to progress further with the understanding of this joint, we must start to approach the subject as Dave Smith has with his thesis project where he so nicely devised a mechanical approach for measuring the lengthening of the arch of the foot to correlate it to hallux and 1st MPJ function. I very much liked the way that Dave did this study and hope that he takes the time to get his research published sometime soon.

    One thing we must do to study FnHL more effectively, and therefore begin to understand it better, is to quit saying "the hallux only dorsiflexes 30 degrees" with no reference to the dorsiflexion force/moment applied to the hallux. Instead we must start to mathematically analyze the load-deformation curves of hallux dorsiflexion (e.g. dorsiflexion stiffness at different hallux dorsiflexion angles, degrees of dorsiflexion for a given plantar load/moment) in order to determine what forces are the cause of this problem. I believe that finite element analysis studies may help us out further in understanding FnHL and I have attached a recently published one that may help inspire others to further research.

    A few years ago, Craig Payne had been working on some research with a hallux dorsiflexion device that measured dorsiflexion angles and dorsiflexion forces/moments and this is exactly the type of reserch that will help us understand the load-deformation characteristics of the first MPJ better. Possibly Craig can comment on where he is on this research and when it will be published.

    I have had an great interest in this subject for the last quarter century and have written quite a bit about it over the last 20+ years in my three Precision Intricast Newsletter books. I have noted the following observations in the thousands of feet I have examined, including intra-operative findings where I have analyzed "windlass function" pre- and post- first metatarsal shortening osteotomies and pre- and post-partial plantar fasciotomies:

    1. Feet with lower medial arches will require greater hallux dorsiflexion forces to cause hallux dorsiflexion than higher medial arches.

    2. Feet with more medially deviated subtalar joint (STJ) axes will require greater hallux dorsiflexion forces to cause hallux dorsiflexion than will feet with normal STJ axis spatial location.

    3. Feet with lateraly deviated STJ axes will often require only a minimal amount of hallux dorsiflexion to allow full range of hallux dorsiflexion.

    4. The greater the plantar load on the first metatarsal head, the greater will be the hallux dorsiflexion force to cause hallux dorsiflexion and the greater the tendency for a restriction of hallux dorsiflexion to occur with a given plantar hallux loading force.

    5. During bipedal standing, a posterior shift of the center of mass will allow less plantar hallux force to cause hallux dorsiflexion than will if the individual leans forward, causing an anterior shift of the center of mass, which will require greater hallux dorsiflexion forces to cause hallux dorsiflexion.

    6. During first metatarsal shortening osteotomy procedures, the amount of hallux loading force required to produce a given amount of hallux dorsiflexion (measured with the plantar first metatarsal head simultaneously manually loaded) is significantly reduced after the first metatarsal has been surgically shortened even a few millimeters.

    7. During partial plantar fasciotomy procedures where the medial half of the central component of the plantar aponeurosis is surgically transected, the amount of hallux loading force required to produce a given amount of hallux dorsiflexion (measured with the plantar first metatarsal head simultaneously manually loaded) is significantly reduced and hallux dorsiflexion is "less-coupled" to first ray plantarflexion than before the partial plantar fasciotomy.

    8. Restriction of hallux dorsiflexion with first MPJ arthrodesis causes an increase in supinated position and/or decrease in pronated position of the foot and an increase in medial longitudinal arch height post-operatively, rather than the medial longitudinal arch lowering and increased STJ pronation that has been previously proposed to occur with a restriction of hallux dorsiflexion.

    9. Lapidus procedures (first metatarsal-cuneiform arthrodesis) will decrease the plantar hallux force required to produce hallux dorsiflexion when compared to pre-operatively.

    From these clinical findings, and from the available research on foot and lower extremity biomechanics, I believe that the whole notion that FnHL is somehow the cause of increased STJ pronation and medial longitudinal arch lowering is untenable, since there is no scientific research that supports this idea. Rather, it is much more biomechanically reasonable for us, as a profession, to progress forward with the idea that the STJ pronation, medial longitudinal arch lowering, increased tensile loading force within the medial band of the plantar fascia, and the resulting increase in hallux plantarflexion moment (that is greater than the hallux dorsiflexion moment from ground reaction force) are the causes of FnHL.

    Hopefully, my few comments here will stimulate further discussion from others.
     

    Attached Files:

  10. Mart

    Mart Well-Known Member

    Thanks Kevin. Your list of observations will give us a useful reference to think about regarding speculation for gait compensations and limitation for what "clinical gait analysis" has to offer on this subject.

    Your point 8 above seems counter intuitive for static measure but explainable for a dynamic observation. is this the case?

    My premises are that in this condition;

    there must be a total loss of windlass action

    and

    unless the foot is actively supinated during late midstance as compensation there would otherwise be loss of "3rd Rocker" ie totally apropulsive gait.

    Therefore your observation refers to a gait compensation pattern rather than a static structural feature.

    Is this a reasonable premise or do you see a better explanation?

    I am nearly finished preparing the case report which I feel interesting because the patient has a unilateral MCJ DJD (natural lapidus of sorts) and a contra lateral plantar heel pain which for what it is worth gives us an interesting intra subject functional comparison.

    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
     
  11. Mart

    Mart Well-Known Member

    I have started a sub thread @

    http://www.podiatry-arena.com/podiatry-forum/showthread.php?p=122931#post122931

    The idea is to keep this current thread of Dave's nice and clean and allow diversion into nitty gritty of using observational video gait examination and cheap/fast/dirty clinical kinetic data for evidence. Also to consider limitations, value and justification for doing this since it may turn out that my example is not that useful to look at Dave's idea.

    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
     
  12. My point #8:

    is a dynamic observation where the patient will walk with a less pronated appearance of the foot following 1st MPJ arthrodesis. The patients have improved propulsion during walking status-post 1st MPJ arthrodesis and often times can run pain free also. However, they may develop increased plantar first MPJ pain due to increased GRF plantar to the first MPJ during gait which can be easily resolved with a foot orthosis with a reverse-Morton's extension.
     
  13. Mart

    Mart Well-Known Member

    Thanks Kevin.

    To clarify and perhaps state the obvious; provided the arthrodesis successfully fixes the joint such that the hallux ground reaction force doesn’t inhibit sagittal motion, the third rocker can work without need to contribute additional compensatory supinatory activity as might be case for hallux rigidus.

    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
     
  14. Martin:

    First MPJ arthrodesis procedures don't prevent the patient from dorsiflexing at the lesser MPJs. As the patient is more supinated in late midstance, more 2nd-5th MPJ GRF occurs so that hallux dorsiflexion become less of a requirement for normal gait.
     
  15. Mart

    Mart Well-Known Member

    Hi Kevin

    Thanks for reply.

    So here is my confusion. One of the main tenants of autosupport is supposedly the supinatory effect of the windlass after HO.

    My assumption is that if anything prevents windlass either something else will need to replace its effect or the normal saggital gait pattern is lost. During late midstance the effect of windlass seems to be an important player in the equilibrium driving inner longitudinal arch behavior AKA Dave's hypothesis.

    With 1st metatarso-phalangeal joint arthrodesis there can be no windlass contribution from the hallux since the metatarso-phalangeal joint becomes fixed in dorsiflexion and cannot exert any force on the plantar fascia.

    Post arthrodesis the hallux may not present inhibiting resistance in the same way as might be expected with hallux rigidus, or to lesser extent with hallux limitus prior to surgery, and as you say the lesser metatarso-phalangeal joints can apply a smaller contribution to windlass.

    For an "equivalent" (to a normally functioning windlass) gait pattern to emerge from this scenario would there not need to be additional active supination applied from somewhere to maintain autosupport?

    Can we speculate that theoretically, if this additional supinatory activity is not provided it might explain your concerns regarding increased 1st metatarsal head ground reaction force needing control with foot orthoses in some situations?

    I guess that fits into the equation which dictates the behavior of inner longitudinal arch height. ie reduce windlass effect on one side but reduce hallux resistance on the other with neutral effect provided the forces have same quantity at same instant in time.

    I haven't read that FEA paper you posted yet. Perhaps that will help me. Can you see any flaws in my reasoning above?

    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
     
  16. David Smith

    David Smith Well-Known Member

    Kevin

    Thanks for your input
    you wrote
    Cheers Dave
     
  17. Supination good :drinks Pronation bad :mad:

    "Auto-support" is interesting. Where does this come from and what evidence do we have to "support" the "auto-support" hypothesis? I've started a new thread on this as not to get in the way here.
     
  18. David Smith

    David Smith Well-Known Member

    Mart and Kevin

    I went back to my raw data and came up with some things that may be interesting

    Below I have inserted a graph showing the stance phase Saggital ankle RoM of the subject of my thesis. The RoM was characterised by the change in relative displacement of the lateral shank V's the lateral border of the foot. (90dgs = neutral position of reference)

    [​IMG]

    In this case the peak sub hallux force did not coincide with peak 1st MPJ force and I find this is usually the case on most plantar pressure observations. It seems the reason that hallux peak force (HPF) was ahead of 1st MPJ (MPF) was that, as mentioned before, the PF positive displacement due to hallux dorsiflexion was greater than the PF negative displacement due to MLA shortening during the propulsive phase. (NB It is important to note that force and not pressure is considered at the sites of interest) The dorsiflexion moments about the 1st met-cuneiform joint (MCJ) were at a peak at 83% stance as was peak total GRF (705ms v's 704ms respectively) At this point the hallux is dorsiflexed by +10dgs relative to the 1st met, which is actually 24dgs because there was a baseline 14dgs dorsiflexion from the 1st metatarsal shallowest angle. A bit of trig using the x ray measurements reveals the heel was about 33mm of the ground by now.

    This then was the most propulsive phase of the gait cycle at the start of contralateral heel contact and double stance phase. If peak GRF, sub hallux force and peak dorsiflexion moments about the MCJ had been much earlier, say before peak sub 1st MPJ force, then this would be well before terminal swing and would tend to accelerate the CoM more vertically or even backwards. At this point it could be argued that a compensation such as cutting short the contralateral swing phase might be utilised.

    So to estimate a good clinical measure of FncHL not being present it may be useful to consider these parameters in terms of plantar pressure characterisation. I.E. that peak hallux force should occur after peak 1st MPJ force and after start of ankle plantarflexion in propulsive phase. Perhaps the peak sub hallux force should coincide with about 10dgs of hallux dorsiflexion after heel off and the contralateral terminal swing / heel contact at around 80% of stance phase. One problem with this last measure might be that if the swing phase shortens then this may always be the case. The propulsive ankle plantarflexion started at around 70% stance, I would suggest that if peak sub hallux force was prior to this then this would significantly inhibit forward progression if no compensation were made.

    Could we devise an experiment based on this. A cohort of say 30 in two groups. Group 1 has inclusion criteria of foot posture in gait that would suggest FncHL and group 2 inclusion criteria that they have gait posture that suggests they do not have FncHL.

    NB - Irony here is that if it were possible to make these two groups then we would not require the experiment since the experiment would only confirm the presence of certain pre determined mechanical conditions and not the existence of FncHL. The conditions for the existence of FncHL would have to be proposed by deductive reasoning, much as I have done above and then applied to the results of the experiment.

    To continue: (the low -ish cost method)

    Use pressure mats (preferably a multi step type) synchronised to saggital 2D video. Record relative timing of discreet plantar pressures of interest and correlate them to the ankle flexion position and contralateral step phase.

    Ho - Clinical observation of foot posture in gait cannot predict the existence FncHL as defined by a priori definition mechanical conditions.

    Ha - Clinical observation of foot posture in gait can predict --etc

    Deductive reasoning - Biomechanical analysis of a priori conditions will give a good indication of the action of forces in terms of excessive ankle dorsiflexion moments early in the stance phase that might lead to pathological stress in tissues of interest. (I deliberatly avoided saying saggital plane perturbation :eek:)

    Correlation of clinical observation with a priori conditions would accept Ha and statistical analysis would show the chances of doing this by chance.

    If Ha is accepted with good probability a further experiment with the same two groups would determine what were the actual moments and powers of interest during the gait cycle of each and did they confirm the earlier theoretical proposition and analysis?

    Them's me thoughts - Now you can all shoot me down in flames :drinks

    All the best Dave

    PS who's a good statistician?
     
  19. Your thesis was based on one subject?
     
  20. I'm not too bad. You've got my number......
     
  21. David Smith

    David Smith Well-Known Member

    Oooooh you are toooo baaaaad!! :)

    BTW the title should have read 'Measures for Identifying changes in 1st MPJ dorsiflexion stiffness in terms of discreet plantar pressures/forces' as it does on my first post - don't know what happened there???

    Dave
     
  22. Yeah, thanks. I don't know quite how to take that, Dave. Take that, take what? Rubbish. Take That and Party? I'd rather eat my own turds, thanks for the offer though. But I have procured "the circus" on DVD for the "better half" as one of her Christmas presents. Yeah- the look on the guy's face in HMV was not even enough for me to say, "it ain't for me fella". What ever happened to proper record shops like in High Fidelity? In which they would have refused to sell it to me, a) because they would not have even stocked it and b) because even if I had walked in with it, then offered to pay for it, they would have piss taken me out of the store in shame? No, all I got was "do you want a bag?" Anyway, Reddington's Rare Records and Ruby Red's smelled of victory and teenage angst. HMV smells of DVD's and sweaty 15 year-olds who's spend too much time playing with their x-box's than music or their selves . "self-doubt and selfism were the cheapest thing I ever bought"- Bunnymen- Back of love. http://www.youtube.com/watch?v=HlvVQZ9Rw3k&feature=related Oh to be 15, again. Look at it, say what it is: HMV... piece of ****.

    Anyway back to the plot...... What's your statistical problem, Dave?
     
  23. BTW, how many subjects were included in your thesis?
     
  24. Dave:

    What I meant to say that this observation would only be apparent during non-weightbearing passive manual examination of the foot, not during gait.

    After first metatarsal shortening osteotomy procedures, the hallux will have less plantar purchase force probably due to the relative shortening of the first ray and resultant decrease in tensile force within the medial band of the plantar fascia during relaxed bipedal stance. The purchase force of the hallux probably comes more into normal range after the osteotomy but I don't have data to confirm this. Also, the medial slip of the plantar fascia may shorten over time. However, since the other slips of the plantar fascia are still under even more tension and they are still attached to the medial slip of the plantar fascia for most of its length, I am not sure how much shortening will actually occur.


    No. What I think happens is that the 1st MPJ arthrodesis procedure greatly increases the first ray dorsiflexion stiffness, since the hallux is fused in a slightly dorsiflexed position, which increases the GRF plantar to the first metatarsal head which, in turn, increases the external STJ supination moment, especially during the late midstance phase and propulsion phase of gait.

    Good discussion.:drinks
     
  25. Mart

    Mart Well-Known Member

    Hi David

    Too much for me to digest in one evenning, but one small observation.

    If you have a chance to look at the FMat spreadsheet data in the gait analysis thread, the IPP and IPF gave opposite result for timing. I guess IPP is confounded by the shape (surface area) of contact and in this analysis not a useful measure. Will get to that in due course.

    I need to spend some time to catch up. I still havent got my head around the FEA paper yet !!

    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
     
  26. David Smith

    David Smith Well-Known Member

    Simon

    Just a throw away retort, no deep meaning.

    You've asked me that before. The answer is just 1. The justification for that was that I used deductive reasoning in place of inductive evidence. Therefore I used and showed a gait and foot that had kinetic and kinematic properties that fell well within the standard normal definitions published. The reasoning here being that if the subject studied has standard normal kinetic and kinematic properties then any discreet action of interest must also be normal. Where normal means; as is universally accepted and expected for non pathological function. By doing this I removed most of the confounding variables that are often not removed when inductive evidence is gathered. Doing this for one subject and repeating the experiment 20 times to show intra subject repeatability and correlation of data of interest took a lot of time in terms of experiment design, novel hardware design, development of reliable techniques to manipulate data and analysis of huge amounts of data. While, as was acknowledged in the thesis, it would have been desirable to use many subjects, there is a time and financial limit to any research and particularly a deadline based project.


    We could start another thread discussing the limitations and shortfalls of inductive reasoning versus deductive reasoning for research of human activities.

    Well, it was a bit of a rhetorical question but, in the theoretical experiment described earlier there would be many variables of interest that would require establishing of the intra and inter variable correlation. I.E. does every foot of interest produce similar timings of discreet GRF and do these correlate with other gait actions of interest? Do they reflect what was expected? How well does the clinical evaluation and expectation match the experimental data?

    Dave
     
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