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Pseudoequinus and DPF

Discussion in 'Biomechanics, Sports and Foot orthoses' started by Phil Wells, Apr 12, 2006.

  1. Phil Wells

    Phil Wells Active Member

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    I have recently been reviewing the discussion on Digital Purchase Force (DPF) due to a group of patients I have recently been exposed to. The group in question are high level Lacrosse players. The biomechanical assessment highlighted that 6 out of 6 patients had psuedoequinus (Forefoot plantarflexed on rearfoot both statically and dynamically) and were reporting symptoms assocaited with low gear/apropulsive 'toe off'. Also tight gastrocs were evident and some other sagital plane restrictions.

    The question I have (Got there eventually) is has any one noticed this type of generic foot mechanics in other sports?
    My thought patterns behind the the causative mechanisms of this foot type in Lacrosse is that rapid plantarflexion of the forefoot on the rearfoot (Going on to tip toes to reach for the ball) results in tonic spasticity of the Gastrocs and associated increased stiffness.
    I assume that this may also occur in basketball and netball (and possibly Oz rules football).

    In one particular player, the flexor hallucis brevis muscles were hyper/hypertrophic possibly assocaited with the very short proximal and distal phalanges of the hallux. Extrapulating from the DPF theory, I am thinking that due to the psuedoequinus, the Dorsiflexory forces of the forefoot on the rearfoot are being 'balanced' by intrinsic muscle activity to maximise the reverse windlass.

    Any extra thoughts on this would be appreciated as I attaempt to develop both orthoses, footwear and training mods to 'sort' things.

    Much appreciated

    Last edited by a moderator: Apr 13, 2006
  2. Phil:

    Digital purchase force is not a theory, it is a fact since the digits do purchase the ground with a varying magnitudes of force. The theory pertains as to why digital purchase force occurs, not whether it does occur. In other words, during quiet bipedal standing, does digital purchase force occur do to passive increase in plantar aponeurosis tension or passive tension in one or more of the other digital plantarflexor muscles, or is it actively generated by tonic contractile activity within one or more of the digital plantarflexor muscles?

    Both John Hicks and I think that the majority of digital purchase force is caused by the passive increases in tensile force within the plantar aponeurosis in relaxed bipedal stance.
  3. Phil Wells

    Phil Wells Active Member

    Terminology discrepency - my most humble apologies.
    However, it brings up the age old question - static verse dynamic - what good is a static explanation when we are primarily dealing with dynamic situations in 'most' clinicaly situations? (I do know there are exceptions or in occupational related podiatry this may be the norm)

  4. davidh

    davidh Podiatry Arena Veteran

    You said:
    "The biomechanical assessment highlighted that 6 out of 6 patients had psuedoequinus (Forefoot plantarflexed on rearfoot both statically and dynamically).

    This does not suprise me. I tend not to distinguish between "pseudo" and common or garden "ordinary" equinus.
    I find pretty much everyone exhibits equinus in one form or another. In fact I do a small experiment on each cohort (usually n=14) of Biomech Workshop delegates I teach. What we do is to agree the definition of equinus, then look for equinus in each delegate. Everyone has it, some more, some less.

    Anyway, practically (and this works in pro-soccer so it should work with your players) I find a 1/8th heelraise on orthoses works well for pretty much all players. I don't know how much room your players have in their sports footwear. Email me if you want info on how to fit a custom orthosis into a small sports-shoe.

  5. Phil Wells

    Phil Wells Active Member


    Thanks for the info but I have an issue with heel raises when the primary mechanism is at the propulsive phase of gait i.e. the rapid plantarflexory force on the forefoot when the person goes on to tip toes. Taking into consideration the pre-positioning abilities of rearfoot posting mechanics, I don't see how heel raises will be appropriate when the forefoot plantarflexion occurs when the heel is non-weight bearing.

    What say you?

  6. davidh

    davidh Podiatry Arena Veteran

    Hi Phil,
    Heelraises don't work particularly well when the heel is off the ground, agreed - but in practical terms they seem to work when the whole foot is on the ground prior to the weight being transferred to the forefoot.

    You've lost me a little here (not hard, some would say), how can you have forefoot plantarflexion when the whole foot is plantarflexed but the forefoot is dorsiflexing due to GRF? :confused:

    Also, in your cohort of patients there will be some frontal plane anomilies... what effect do these have on the symptomology?
  7. Phil Wells

    Phil Wells Active Member

    The idea is with the tip toes position is that the 'person' generated plantarflexory forces are greater than the dorsiflexory forces due to GRF. I assume that the PF forces are being generated by tricep surae activity - possibly both concentrically and eccentrically (On/off action), flexor contraction and reverse windlass. The question may be how much of the digital purchase force is muscle activity and how much ligamentous resisitant/increased stiffness (possibly due to rate of loading mechanics and muscle activity). This is important as it will change my intervention approach.

    The frontal plane abnormalities are usually present via a flexible lateral column and/or pf 1st rays. The greater these, the more symtoms seem to be reported proximally up the limb - the more distal the abnormality from the ankle joint, the more of a lever effect the foot has on medial/lateral rotation of the leg.
    i.e. moments generated across the subtalar joint are greater and consequently transfered to the shaft of the limb.

    I think this make sense (in my world anyway) but please feel free to challenge anything I have said.


  8. Phil:

    Static situations are helpful in understanding dynamic situations in many cases. Static analysis allows one to use simpler analysis techniques, such as the free-body diagrams I used in Thought Experiments #1-6, to model the internal forces within a structure, such as the foot. Dynamic function, of course, is more complicated. However, in my 20+ years of studying and teaching static analysis and then applying these concepts toward the dynamics of various weightbearing activities, I have found that both my knowledge and my students' knowledge have been greatly increased as to what may be mechanically occuring within the foot and lower extremity during dynamic situations.
  9. Phil and Dave:

    Interesting discussion. In a static situation, with the feet flat on the ground, digital purchase force (DPF) will be increased with any increase in plantarflexion moments at the metatarsophalangeal joint (MPJ). DPF may also be increased with an increase in plantarflexion moments at the interphalangeal joints.

    However, in the dynamic situatoin of raising up onto the MPJs in a "tiptoe" position, the increased contractile activity of the gastrocneus-soleus complex (GSC) will cause an increased ankle joint plantarflexion moment and a plantarflexion acceleration at the ankle. This will, in turn, cause the heel to lift from the ground, and simultaneously, cause the MPJs to dorsiflex.

    The MPJ dorsiflexion during this maneuver is caused by an increase in GRF plantar to the digits (i.e. increased DPF) which will then cause an increased MPJ dorsiflexion moment and, if the MPJ plantarflexion moments remain relatively constant, will cause a dorsiflexion acceleration of the MPJs. If the MPJ plantarflexion moments increase at the same rate as the MPJ dorsiflexion moments, no digital dorsiflexion motion will occur. This common clinical scenario is the biomechanical cause of hallux rigidus, hallux limitus and functional hallux limitus. If dorsiflexion of the digits do occur with heel rise, this is usually a completely passive dorsiflexion motion at the MPJs, with all the dorsiflexion moment coming from the increase in GRF plantar to the digits that results from heel rise and ankle plantarflexion motion, with no MPJ dorsiflexor activity necessarily required.

    This increase in DPF (or increase in GRF plantar to the digits) may result from multiple sources during the heel rise maneuver. When attempting to determine which structure contributes the most to this increase in DPF with heel rise, the problem is that this can not be easily solved since there are so many sources of potential increases in DPF with the heel rise maneuver. Here are a few potential sources that may cause an MPJ plantarflexion moment during the heel rise maneuver that may, in turn, cause an increase in DPF:

    Each of these anatomical structures can exert a MPJ plantarflexion moment on the digits so that either DPF is increased, or if the MPJ plantarflexion moment is increased enough, or so that MPJ dorsiflexion motion is stopped or prevented from occurring. I don't think we have any way currently of knowing in the international biomechanics community just how much each structure is contributing to DPF. Therefore,one needs just to take an educated guess based on the mechanical characteristics of the foot that is presenting to you at that time.
  10. davidh

    davidh Podiatry Arena Veteran

    You said (much cut):
    "The question may be how much of the digital purchase force is muscle activity and how much ligamentous resisitant/increased stiffness (possibly due to rate of loading mechanics and muscle activity). This is important as it will change my intervention approach."

    I understand what you are saying here - I think, though, that it is impossible to generalise about your approach to your cohort of players since there are simply too many unknown variables.
    Unless your players routinely use Astroturf (perhaps they do), the supporting surface will not be uniform. Then there are the frontal plane anomilies I suggested some of your players will present with. Then there are the different degrees of joint ROM which we can generally find even in a relatively small cohort.
    I didn't even mention diurnal variation :D .

    You said (much cut):
    " I don't think we have any way currently of knowing in the international biomechanics community just how much each structure is contributing to DPF. Therefore,one needs just to take an educated guess based on the mechanical characteristics of the foot that is presenting to you at that time."

    To which I completely agree.

  11. Phil Wells

    Phil Wells Active Member

    Thanks for the reply. I have a couple of quick questions.
    What do you mean my the term acceleration - is this an actual movement or a potential one - sorry havn't been exposed to this term in foot mechanics and I want to make sure that I totally understand what you mean in relation to this subject. I assume you mean an actual movement where equilibrium is not in effect.
    Secondly, you speak about dorsiflexion of the Mpj's when the ankle is plantarflexing but does this have to happen i.e. if the plantar ligaments and tendons are stiff (Hypomobile etc) will they resist this movement?


  12. Acceleration is a standard term used within physics and biomechanics to describe a change in velocity of an object over a certain period of time. Acceleration is calculated as the change in velocity divided by the change in time over which that change in velocity occurred.

    For example, if a coffee mug is resting on a table and then you push the coffee mug across the table with your hand so that the end of one second of motion a velocity of 0.1 meters/second (m/sec) has been achieved, this movement from rest (velocity = 0 m/sec) to a new velocity (velocity = 0.1 m/sec) has resulted in a change in velocity of 0.1 m/sec. Therefore, the average acceleration of this coffee mug would be 0.1 meters per second per second (m/sec^2).

    Acceleration for translational movements (i.e. from point A to point B in a straight line) is generally called linear acceleration. However, acceleration of an object around an axis of rotation is called angular acceleration. For example, during propulsion, let's say that the metatarsophalangeal joints (MPJs) of a foot go from a resting position before heel off (angular velocity = 0 degrees/second) to a new dorsiflexion velocity of 120 degrees/second over a 0.2 seconds time period. The average MPJ dorsiflexion angular acceleration would then be 600 degrees per second per second or 600 degrees/sec^2.

    Therefore, open up any high school and/or college physics book, read about acceleration, and this is how "accleration" is used within the international biomechanics community and within my earlier discussion on digital purchase force.

    In my earlier posting, I discussed this scenario as follows:

    In other words, if there is some internal force acting across the MPJs that increases in magnitude along with the increase in GRF plantar to the digits during dorsiflexion (e.g. what you call the "plantar ligaments and tendons are stiff"), then, yes, the MPJs will not move into dorsiflexion during propulsion.

    For example, let's say, in the case of functional hallux limitus (FnHL) that GRF acts plantar to the hallux at a moment arm that is 4.0 cm distal to the 1st MPJ axis. At the time just prior to heel off, GRF plantar to the hallux is 20 Newtons (N), and GRF increases to a value of 80 N when the plantar heel has raised 3 cm off the ground. However, it is noted that during this rapid 4 fold increase in plantar hallux GRF that the hallux has not dorsiflexed at all at the 1st MPJ. Since no 1st MPJ dorsiflexion motion has occurred, then we can apply the physics principle of rotational equilibrium to the 1st MPJ in this example.

    Therefore, the 1st MPJ dorsiflexion moment has increased from 0.8 Nm (20 N x .04 meters = 0.8 Nm) at the time of heel off, to a value of 3.2 Nm (80 N x .04 m = 3.2 Nm) when the plantar heel is 3 cm off the ground. We can therefore be absolutely certain that the internal 1st MPJ plantarflexion moments have also increased from 0.8 Nm at the time of heel off to 3.2 Nm when the heel is 3 cm off the ground.

    How can we be so absolutely certain of these values? We can be certain because the hallux has not moved at the 1st MPJ from just prior to heel off to the time the heel is 3 cm off the ground, and, as a result, rotational equilibrium across the 1st MPJ axis has been preserved. If we now assume that the plantar ligaments and plantar fascia and plantar muscles are the cause of this 1st MPJ plantarflexion moment, then we know that the tensile forces within these structures have also increased, on average, 4 fold, since the 1st MPJ plantarflexion moment they produce has risen in magnitude from 0.8 Nm to 3.2 Nm. In other words, if we assume that the plantarflexion moment arm for these plantar structures is, on average 1.5 cm plantar to the 1st MPJ axis, then we now know that the plantar tensile force increased from 53.3 N at the time of heel off to 213.3 N when the heel is 3 cm off the ground. In this way, in FnHL, if the increase in GRF plantar to the hallux during propulsion that tends to cause hallux dorsiflexion is counterbalanced by an equal and opposite tensile force acting plantar to the 1st MPJ axis that tends to resist hallux dorsiflexion (i.e. 1st MPJ plantarflexion moment), then rotational equilibrium will have been maintained at the 1st MPJ during propulsion, hallux dorsiflexion will not have occurred, and, as a result, FnHL will have occurred.

    In conclusion, the lack of 1st MPJ dorsiflexion motion during propulsion may not necessarily be due to the plantar ligaments and plantar tendons/muscles being "stiff" as you say, Phil, but may be due, as in the case of FnHL,to the medial longitudinal arch height being so low and the subtalar joint axis being so medially deviated, that this increase in tensile forces within the plantar ligaments/tendons/muscles does not produce their usual increase in medial longitudinal arch height that would then be more likely to allow hallux dorsiflexion to occur during propulsion.

    Hope this rather lengthy explanation helps yours and other lurker's understanding of this complicated but important mechanical concept.
  13. Phil Wells

    Phil Wells Active Member

    Thanks for the info re acceleration. As you said, the definition of acceleration is VERY basic and I was a bit ingenuos when I asked for a definition. This was mainly to ensure in my own mind that we were all using the same terminolgy as our profession is loaded with the mis-use of biomechanical terms and mis-understanding. I assumed you were using acceleration correctly but as you ommitted to define angular verse linear types in your 1st posting I thought I had better be sure. Again thanks.
    I personally included the rate of acceleration in my patient assessment as it is important to the understanding of pathomechanics. An example would be the tib post tendinopathy verse tib post muscle dysfunction. I have found that where rapid loading of the tendon eccentrically is present , the pathology is primarily one of the tendon. However where the tendon loading is slower, the muscle pathology is primary.
    Does this make sense or am I seeing patterns that don't exist?

    Re your explanation of rotational equilibrium applied to the MPJ' s, many thanks as it indeed is a fundamental part of foot mechanics and it is nice to see it applied to something other than the STj in a clear and meaningfull manner.


  14. How do you determine whether rapid vs. slow PT tendon loading is occurring?
    Are you doing electromyography on these patients or are you somehow measuring the strain or tensile force within the PT tendon?
  15. Phil Wells

    Phil Wells Active Member

    As was mentioned earlier, a best guess is used based on loading characteristics - e.g. running speed. I assume that if acceleration increases, then the rate of loading of a tendon will also increase. I also assume that the stiffness of the tendon will also increase as loading of the tendon also accelerates/increases.
    Also the presence of fatigue in a muscle tends to change the tendon loading properties. I always assess my patient pre and post exercise to determine if fatigue is the causative pathomechanics. I have been caught out by a patient in my earlier clinical days and found due to both tonic spasm in an antagonist and gait related weakness in the angonist, the lower limb mechanics were very different post activity.

    As ever, the need for accurate measurement is the ideal but until then, I rely on theories that make sense.


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