Rate/Velocity of Pronation

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A few comments in another thread got me thinking about this.

My basic understanding of this has always been that viscoelastic materials (such as most human tissues) are strain-rate sensitive. i.e. The quicker they are loaded -> stiffer they become -> higher tensile loads developed.

What are others thoughts on this? And if people are regularly considering pronation rates/velocities how are they 'measuring' them?

Ian

 

Not a direct answer to your question, but this whole concept of rate of pronation is an interesting one. How often have you heard people say (and they often lower the tone of their voice or whisper when they say it, likes its a big secret) something like "its not really the amount of pronation, but the velocity of pronation". I love asking them "How do you know that?" ... they have no idea!!!! That does not mean it isn't, its just the way they prononce it as though its some sort of hidden secret that is the truth, that they are revealing!

Intuitively, yes, the rate of motion is a factor, as it takes more effort to stop it if the rate is high --> greater risk for tissue damage --- the tissue stress model

 

no sure which law number it is, but Newton a smart man said

Force = mass* acceleration.

so as important as the amount of movement, direction of movement is speed. The more speed the greater the load on muscle and therefore very important I beleive in tissue stress.

The 3 basic actions of muscle is the accelerate, decelerate and to stabilise. So joints movement that is quicker will take more force to decelerate therefore more tissue stress. I tend to think mostly about this when considering resupination of the foot especially in flexiable pes cavoid foot type.

Michael Weber

 

Michael,

I agree with you, and with Craig - there is no doubt that the application of Newtonian physics (thats his 2nd Law by the way ) and also engineering principles makes theoretical sense, particularly to a tissue stress model subscriber.

What I'm asking is how you 'measure' or quantify this clinically?

Ian

 

Hi Ian at the moment I don´t think we can. Ive been having this conversation with one of the guys who had the pins screwed into his legs and feet in sweden. I´m not on the work computer so don´t have the exact title but in vivo running something with Nester and Arndt being 2 of the people involved.

Anyway we were discussing how their research will be used clinically and i mention the rate of pronation and the response was it can´t be measured clinically at the moment.

But I beleive that we can work along the lines that certain foot types will have to move faster to complete movement during the gait cycle. Not much science I know

Michael Weber

 

Just found these threads while doing a bit more reading:

Evidence for velocity of pronation and injury?
Orthoses and pronation velocity

 

I don't think that it's the rate of pronation, but the stopping of pronation that causes pathology. It doesn't hurt to move the joint fast as long as the stopping of motion has lower forces. True, that hitting the wall, or the floor of the sinus tarsi, at high velocity will require higher forces than hitting the end of range of motion at low velocity.

However, the factors that tend to cause high velocity will be the same as those that will cause high forces in a static situation. Moment = moment of inertia times angular acceleration. So a high pronation moment from the ground will tend to cause high pronation velocity. In static stance a high pronation moment from the ground will cause a need for a high supination moment from some anatomical structure like the floor of the sinus tarsi. Either way, you would tend to treat the problem by attempting to reduce the pronation moment from the ground.

In the case of a weak posterior tibial muscle, you could get a high pronation velocity in the presence of an average pronation moment from the ground. In this situation the pathology causes the high pronation velocity rather than high pronation velocity causes the pathology.

To use the tissue stress approach you have to think about the specific anatomical structure and then look at what factors will reduce the stress on that structure. Velocity is one factor, and not necessarily the most important factor, that will effect forces on a structure.

Cheers,

Eric

 

Eric,

This is a good point -> motion does not hurt, its the forces stopping the motion which are (potentially) pathological. Craig used a cool analogy at the London bootcamp which I have repeated many many times since: 'Falling off a building does not harm you, but the ground which stops you falling does'.

Ian

 

From the time when the first studies which demonstrated that it was rate rather than amount that changed with foot orthotics, it seems as though explanation after explanation was required in an attempt to jive this finding with prior theory.

If it is the rate of pronation that is the issue, then why is it that the "pronation" we have always related to pathology occurs in the 2nd half of the single support phase (ie, late midstance pronation)....and not during the contact phase when STJ pronation is actually a normal, accommodation to internal rotation of the striking limb?

Looking at pronation as a contact issue misses the elegance of the body's ability to raise its own weight during walking. When it fails to raise its own weight, pronation during midstance is the accommodative result.

Howard

 

From a tissue stress/biomechanics/engineering perspective, the late midstance pronation we commonly see during gait is not so much a failure of the body "to raise its own weight", but rather is due to a decrease in medial longitudinal arch stiffness (i.e. increased deformation of the medial longitudinal arch for given plantar forefoot loading force incease). Feet that have decreased medial longitudinal arch stiffness will exhibit increased flattening of the medial longitudinal arch with the increasing plantar forefoot loading forces that are inherent in human bipedal gait during the late midstance phase of gait. This abnormal but common gait finding of late midstance pronation is very simple to understand using this mechanical explanation, without needing to worry or consider whether or not the body can raise its weight during walking. In addition, those feet that have this decreased medial longitudinal arch stiffness will also develop lower medial longitudinal arch height at the end of late midstance phase of gait which will, in turn, tend to cause functional hallux limitus during gait during propulsion.

 

here is the paper is was referring too.
Intrinsic foot kinematics measured in vivo during
the stance phase of slow running
A. Arndta,b,, P. Wolfc, A. Liud, C. Nesterd, A. Stacoffc, R. Jonesd,
P. Lundgrena, A. Lundberga

If you look at the motion of the individual bones its amazing to see how little they move. If we take the navicular and Tib Post instead of a large movement as ´pronation´

Nav—talus
Sagittal 6.5 (2.9)
Frontal 13.5 (4.1)
Trans. 8.7 (1.4)

Cub—nav
Sagittal 5.5 (2.0)
Frontal 5.5 (2.0)
Trans. 5.6 (1.8)

Cun—nav
Sagittal 7.1 (4.0)
Frontal 8.1 (2.6)
Trans. 4.1 (1.1)

these are the mean readings from the research.

Now if you read the paper they moved at approximently the same speeds and there was differences recorded between stubjects so this indicates that the joint motion occured at a faster rate therefore more force applied by the navicular to the tib post during drift and drop.
We are of course talking about degrees and seconds. What would be intersting would be also have the a measurment of pull on the tib post tendon in relation to the rate of navicular change in these patients to give some more to think about.

Michael Weber

 

Michael,

It would be much easier for others to read an article you have recommended if you reference it correctly

Or provide us with a link

Ian

 

Sorry Ian still working out how to do things with links etc here is the full title.

Instrinsic foot Kinematics measured in vivo during the stance phase of slow running A. Arndt, P Wolf, A lie, C Nester, A Stacoft, R Jones, P Lundgren, A lundberg Journal of Biomechanics 40 (2007) 2672-2678.

I see that your link take people to the article.

Michael Weber

 

Kevin,

And with a decrease in arch stiffness, there is an inability to raise body weight. The missing effect is the neurological response to weight moving in the wrong direction at the wrong time during the gait cycle. It is very useful to apply engineering principles to the body in motion. It is, however, the timing of these events in the presence of poorly coordinated muscular response that comprises the basic elements which ultimately create the clinical syndromes which we are charged with managing. Babies are not built in a factory.....and as such, the inter-connectivity of the mechanical and neurological systems cannot be ignored.
Its great to simply explain the stiffness issues of the midfoot....but without a different understanding of how this effects the "gait continuum"... it is too foot centric to see the impact on the entire body.

Howard

 

Howard:

I don't believe that by trying to simplify the understanding of the gait finding of late midstance pronation by describing it as a result of a decrease in medial longitudinal arch (MLA) stiffness "ignores" the inter-connectivity of the mechanical and neurological systems of the individual. In fact, the degree of MLA stiffness that any individual's foot displays is at least partially determined by contractile activity from the peroneus longus, flexor hallucis longus, flexor digitorum longus, posterior tibial and plantar intrinsic muscles, all of which, in turn, are under direct control by the central nervous system. A failure of any of these muscles to contract forcefully enough to create increased stiffness in the MLA during late midstance may lead to late midstance pronation and, therefore, may be thought to be due to central nervous system effects. This combination of engineering and physiology knowledge will be the way forward for us to gain a better understanding of the biomechanics of the human foot and lower extremity in the coming decades.

 

Micheal

You said F=MA and then said so its the speed and direction of movement that matters. So you are talking about velocity which is not an acceleration. Velocity alone is not in the equation of force only rate of change of velocity i.e. acceleration. There must be acceleration to produce force and vice versa.

This may sound pedantic but it is not. It has been proposed that the acceleration that tends to cause pathology is the braking/deceleration, which is actually acceleration.

So if the velocity of a certain limb is high but the braking to zero velocity is over a long period then the acceleration is low and so is the peak force. If the same limb with the same mass has the same velocity and it brakes over a much reduced time then this will equal high acceleration and increased peak force.

This is not the whole picture though, since the force integral in both cases may be the same. I.E. the latter has a high peak for a short time the former has a low peak for a long time but if we plot this as a time force curve then the area under the curve will likely be the same.

The relationship of pathology to force integral is not well known (as far as I know) and this is similar to pressure induced pathology, which, of these two are worse? high pressure for a short time or low pressure for a long time? or is it some thing in between these two parameters?

Converting to pressure is not as spurious as it may seem, force in a tissue is expressed as stress and stress is measure of force per unit cross sectional area (CSA), which is very analogous to pressure. Therefore a tissue with a large cross sectional area has lower stress than a tissue with small CSA for the same force load. The rate of change of tissue loading would be analogous to rate of change of velocity of the limb containing that tissue of interest. Therefore identifying the nature of the internal stress or pressure/stress integral of a certain tissue of interest in terms of pathology potential would be useful but so far unknown.

An example;

If the STJ pronated at a high velocity and was braked by the ground at a high acceleration but the area of ground foot contact that produced the force for supination moments was large then the stress in the plantar tissues might be quite small but for the whole period of the stance phase.

However if the STJ pronation was not such a high velocity but the pronation was stopped by the force from the post tib muscle tendon producing supination moments then the stress in the Post tib tendon which has a small cross sectional area, compared to the foot, might be quite high even if the braking / acceleration was slower than the former example.

Perhaps you can see from this example that it would be difficult to predict a proportional correlation between STJ pronation speed and injury potential.


Of course there are several parameters of the action of the foot during the stance phase which have limited variables. Therefore it might be intuitive to think that increased speed would equal increased acceleration and therefore forces but, I think, these assumptions must be approached with caution especially when considering them in terms of injury potential and in terms of stress integrals.

Regards Dave

 

Thanks Dave, I see what your saying

The above could be worked in a great mission statemant for study. Do you know of a machine which measures the internal stress placed on muscle in both eccentric and normal muscle contractions.

Michael Weber

 

Michael

The way to directly test muscle/tissue strain (change in length due to load) is to attach a strain gauge to the muscle/tendon of interest. Of course this is fraught with difficulties.

Indirectly you could use finite element analysis, this has many limitations based on knowledge of the anatomy and physiology and composite structural engineering properties of the living body segment of interest.

New methods using MRI in conjunction with the above are being tried. One major obstacle is that tissue / material properties in vivo are completely different to in vitro and to get accurate data from the FEA models first one needs to know the material properties of the tissues of interest.

Even when this is done the experiment that would define the rate of load over time to injury rate ratio would be very large and long and probably difficult in ethical terms.

I expect that defining tissue pathology due to loading rates will be something that would eventually be an analysis done by computer modelling and not in vivo.


Cheers Dave

 

You can't know the tension in a tendon just by looking at velocity. Net moment = moment of inertia x angular acceleration. If there was a high pronation moment from the ground and a not quit so high supination moment from the tendon then there would be a small net moment and a relatively small acceleration in the direction of pronation. So, you can have a slow velocity of motion with high forces on the tendon.

There was some articles written by Komi on placing of force transducers on tenodns. The difficulty of this approach is finding subjects (and ethics committees) willing to have force transducers surgically implanted on their tendons. That is why we move to mechanical modeling. There is a good article on this by Morlock and Nigg. Sorry don't have time to dig up cites right now.

Regards,

Eric

 

Kevin,

I have been giving some thought to your prior responses to this issue. I think we have diverging views because of how we view gait changes with orthotics. In the many years I have used in-shoe pressure testing, I have come to the point where I seeing the practice of podiatric biomechanics as being "all about weight" and its ability to effectively transfer from proximal to distal during any particular step. It is remarkable how little needs to be done in orthotic posting, shell design, etc when one measures the weight transfer changes vs. when simply "eyeballing" how much "pronation" one sees during walking or standing. At this point in my career, it seems that by the time one creates a "visible" change to joint position, the patient has been overcorrected.

Howard

 

Howard:

Since our methods of assessment are different, then certainly it would make sense that our goals of orthosis therapy may also be different. From what you say above, when you observe a change in joint position with foot orthoses, you determine that this is negative for a patient, since this would mean the patient has been "overcorrected". Rather, from my clinical perspective in many of my patients, if I do not see a change in foot and lower extremity kinematics during gait, then I feel that my patients are "undercorrected" with my foot orthoses.

Changes in joint kinematics within the frontal plane, such as having the orthosis alter the subtalar joint function to a more pronated or supinated position, is not always my goal of treatment. However, in many cases, such as in the foot orthosis treatment of posterior tibial dysfunction or chronic peroneal tendinitis, if I don't see some kinematic change in subtalar joint position/motion, then I will likely try to add more "correction" to my orthosis. In other cases, such as the treatment of proximal plantar fasciitis, then I would agree with you that I am not so much looking for changes in frontal plane subtalar joint function but rather am more interested in how the orthosis reduces the patient's pain, and making sure the orthosis is not producing abnormal gait patterns or causing pain or symptoms elsewhere.

I don't think we are too far off from each other in our goals for our patients, Howard, since we both want the best for them. The assessment and treatment methods that allow us to arrive at these goals are obviously different, which, I believe, is good for our patients (and good for podiatry), since it provides alternative methods by which other clinicians may achieve the therapeutic goals that patients desire.

 

Howard,

I don't think that we are that far apart. I agree that a lot of patients who don't need have a change in position or motion to get pain relief. I also agree with Kevin that there is a subset of patients who do need motion changes to see releif.

I also agree that measuring the "progression of weight transfer" could be a very good measure in predicting orthotic success. We just need a protocol that anyone could use to prove that it is successful. Just as we need a protocol to prove that the tissue stress measures can be successful.

Regards,

Eric

 

Hi Howard

When you're using FScan to determine when you have done enough with an orthotic, what exactly helps you determine the point that you've done enough? As someone new to FScan, I'm interested to know which parameters you find most useful (COF trajectory, F/T curves, plantar pressure changes, CoM'nalysis). Is a bit of a change in these parameters what you're after or is their an ideal that you're looking for?

Rebecca

 

Rebeca,

The key determinant for evaluation of pressure during F-scan is the shape of the force/time curves. I usually use 3 "object boxes" (these are specific areas which can be masked to determine pressure in their locations over time). These sites are the total footprint, and then the heel and forefoot (usually not including the digits).

During gait, these pressure should rise and fall in a smooth, gradual fashion (double hump appearance). If there are periods of asymmetry, or areas in which these curves level (ie, stop rising or falling), then some type of motion restriction has occurred. Orthotics can be modified and retested to see if this leveling has changed. Heel lifts can be used to resolve asymmetry (as long as it correlates with other clinical exam findings of LLD). If there is asymmetry but no clinical evidence of LLD, try using a thin poron (PPT) heel lift to "slow down" the faster moving side.

Hope this helps. I am a bit crunched for time now....If you have further questions, I will try to get back to you after this upcoming weekend.

Howard

 

Hi Howard,

I think you and Tekscan could be more specific about this. "Smooth gradual fashion" is not very informative. If F/T curves are valid measures, why can there not be reference to normative measures? A F/T curve can be defined by the amplitude (y axis) of the peaks and trough (as a percentage of body weight, which is unfortunately not available with FScan), and by the timing (x axis) of the peaks and trough.

Surely smooth gradual and even symmetrical curves, without defining the above characteristics, cannot necessarily mean its a normal or ideal F/T curve. Should the peaks (rearfoot & forefoot) be of the same amplitude, is it OK if the first is a bit higher than the second, or vice versa? Should the peak be half or 3-quarters or four-fifths the amplitude of the peaks? What is the timing of the peaks that is normal / ideal?

Regards

Rebecca