Lateral STJ instability with restricted internal hip RoM

Thanks all for your input,

It is my opinion that restricted internal hip rotation will tend to result in increased supination moments about the due to external rotation of the leg as the hip of the standing leg internally rotates during contra-lateral swing. The reasoning is sound and the observation is consistent with the reasoning. Having said that the observation of kinematic change is foot supination thru stance phase only tends to occur if the restricted internal hip rotation is concomitant with lateral stj axis or valgus f/foot, e.g.The balance of moments falls on a plus side for supination - if the STJ axis is medial then the pronation moments may be too high for there to be a visual kinematic change to be affected by supination moments due to external leg rotation moments. In this later case there may be for instance a shortening of the step or external foot placement (toe out) as compensation. The supinating foot is only one possible outcome of restricted internal hip rom. The restricted RoM I talking of is where the hip has very stiff or no internal rotation available past where the knee is straight ahead in the direction of progression.

Regards Dave

 

Only infrequently do I make foot orthoses for asymptomatic people and these people mostly want orthoses because their old orthoses are becoming broken down and don't want a return of their symptoms. That being said, every now and then I get a child with significant flatfoot deformity that has no symptoms but has gait abnormalities that I recommend orthoses for. In addition, sometimes I get an adult patient with flatfoot deformity that wants orthoses but is asymptomatic, and generally I recommend over-the-counter foot orthoses for them.

That being said, in my practice now of 31 years, where I am making about 70-80 pairs of orthoses per month, the key factor which determines whether a patient gets custom foot orthoses or not is their symptoms and whether or not their symptoms are being mechanical in nature or not. I wouldn't recommend foot orthoses for patients with abnormal gait examination findings without symptoms unless I thought those abnormal gait findings would cause harm to the patient over time. In other words, the presence or absence of symptoms (i.e. subjective complaints) are still the key to whether I recommend foot orthoses for my patients or not.

 

I am going to reply in more than one post to keep things separate.

You are of course correct that we cannot measure internal tissue stress but no system can do that in the way you describe. Joint moments are the closest we get but these are a combination of the force applied and the kinematic position which is what we are describing albeit without calculating the moments.

However, you raise a VERY interesting point. We also measure the velocity of a number of these variables. You referred to reducing the excursion and this may be due to an internal braking force - calculated joint moments will not tell you this - but I wonder if the a change in the velocity of motion may give us an idea as to the load a change may be placing on the internal tissues. I will need to give that some thought.

With regards the use or not of Orthoses. In my case, we saw no change in the forces with a range of Orthoses and subsequently no change in the kinematic function. It was therefore my opinion that the Orthoses are less likely to provide any benefit as one could deduce we have not changed the joint moments.

This was supported (based on the agreement that subjective feedback is key) by her stating that despite the Orthoses being comfortable (i.e. she was more comfortable with then without), her presenting symptoms were unchanged.

So why bother and not simply give the Orthoses. If I had provided Orthoses on my clinical assessment (btw what SALRE approach do you take for hip and pelvis pain) and it had not helped, some may have modified the prescription and assessed that benefit. In my opinion, we explored the changes possible on plantar forces with a range of options, then the general effect on the proximal structures and saved her time, and some money on pursuing custom orthoses that would have no benefit.

T

 

Something that has occurred to me in this discussion which I should clarify is what we measure kinemtatically ? we are assessing ankle to pelvis measures, we are not using a foot model. Patients are tested with shoes +/- orthoses and comparing shoes. Whilst we could use shoes with windows etc., the analysis takes on another level and becomes less practical for clinical use.

Thus, when I talk about changes, these are generally more proximal. I do believe that tibial rotation is a variable that we have not considered as we cannot make any assessment without 3d. I see this consistently change with orthoses and footwear. This is where I then look to what is in the literature. The work from Nester?s group indicates that, if anywhere, tibial rotation couples with arch height. Thus, if we use orthoses with any form of effect on the arch, or shoes with differing levels of flexibility / resistance in the arch, we have the potential to effect the arch and thus tibial rotation. Whether you like comparing to a normal range or not, we can assess if the movement increases or decreases and the range (rather than a distinct average) can guide as to whether the motion is a little more excessive or a little more restricted.

I think medial knee oa is a good example of the issues. The literature tells us that there are increased medial knee moments and laterally posted orthoses reduce these moments. I am sorry, but I do not have the references to hand but one systematic review demonstrated that up to 30% of patients do not get symptoms relief form this approach. Resende et al have recently demonstrated the effect these types of orthoses have on the whole lower limb and suggest we have some caution.

I have seen two cases of late who had excessive tibial rotation. When I assessed navicular drop / drift, I felt this was increased and it appeared coupled. I trialled an OTS device to simple reduce arch motion and immediately, in clinic on single leg squat, he had an 80% reduction in symptoms, supported by7 feedback at review.

This meets the subjective criteria but my approach to management was based on the findings of the gait, my clinical examination, an understanding of the literature that relates to joint coupling and the practical application.


This is one example of a condition where I see more than one pattern of dysfunction for a single pathology and this makes sense given that we demonstrate 3d motion. It also goes some way to explain why it is difficult to demonstrate links in studies that look at one condition; if there are more than one combination / patterns of motion, this would get lost in statistical analysis.

By analysing a range of pathology clinically, we may be able to identify patterns that can then be researched appropriately.

T


Resende et al Ipsilateral and contralateral foot pronation affect lower limb and trunk biomechanics of individuals with medial knee osteoarthritis during gait Cl Bio, 34 (2016) 30-37

 

Kevin noted:

The problem then is if one is only using an in-shoe pressure analysis system which doesn't measure shear forces, does not provide the spatial location of the GRF vector during gait and the STJ axis location is not known, then it would be impossible to reasonably predict whether the interosseous compression force within the sinus tarsi is being reduced, unless, of course, the foot is seen to supinate out of its maximally pronated position during gait.

There are simply too many variables which are unknown to allow us to predict internal forces within the foot and lower extremity even within the most advanced biomechanics lab setting. That is why we must, as clinicians with our basic analysis tools, use the subjective comments of the patient combined with our gait analysis findings (i.e. kinematic data) to do our best to predict whether the mechanical interventions we are making for our patients are therapeutic, or are harmful

If I am correct, this is the gist of your argument as well.

So, there are some points here:

1. Kevin refers to gait analysis (i.e. kinematic data), well we can do that visually and the more experienced will pick up more than the less but, is there any reason this cannot be obtained more objectively?
2. There are aspects of kinematic evaluation you cannot evaluate without 3d (i.e. rotation).
3. As a tease, if this is the case, is there any point in research using any of these techniques?
4. If someone chooses to use orthoses based on the Root theory (or at least the structural basis of Root) and they get symptom relief, why is this wrong given that we cannot assess function? The patient does not care and most of the orthoses modifications used can be linked to a structural approach. I am not saying I agree but, by the same token, what is good for the goose?
5. If we take the literal interpretation of this, there is no way of assessing function adequately as our measuring tools are insufficient. Thus, the only gauge is symptom relief or not. Thus, it is not possible for anyone to state that they have reduced load on a structure without loading another structure or adversely affecting gait? you do not know that.

The last point has always been the issue I have had with the tissue stress relief approach, no-one has ever demonstrated how they know the intervention they have provided has not caused stress elsewhere other than it did not start hurting. Well I see plenty of ops that have shortened the first ray and they develop symptoms but usually at least 2 years later or longer ? patients rarely link the two. No-one has ever taken an approach to look at symptoms patients have developed 2+ years after orthoses to my knowledge. We do not know. We would get castigated if we did not know our complications surgically ? how many know their complications from orthoses?

At the end of these posts, I suspect I have not answered Simon?s questions. I fully accept the limitations you indicate, the need for further research etc but do not necessarily agree the approach has limited merit and believe it can further our understanding.

My over-riding drive has been three fold:

1. To help my patients as much as possible.
2. To further my understanding
3. As importantly, look to develop a process that lends itself to teaching. The assessment of forces and moments, the application of control to modify load are all aspects that can be taught. The effect these forces have and how you manage patients when things do not work or they do report other symptoms is something that is left to experience. We need to do better than that.


T

 

Trevor,
Thank you for your well considered responses. I'll start with your first, but I have to go work a clinic this morning and then we're off BMX racing for the weekend. I'll come to your other points as time allows over the next few days.

Agreed, but we need to be open and aware of the limitations here. As Kevin pointed out, we can't gauge the net ground reaction force vector from the in-shoe pressure system and we don't know the axial positions. Don't get me wrong, I understand that the technology is useful, but at the same time we have to be aware of what it can and can't tell us. I know you understand that, but when we write here, we need to try to ensure that all the others following the thread are cognisant too.

Yep, that's an interesting one and I'm glad you picked up on it. Obviously, force= rate of change of momentum, the faster the momentum of a moving body changes the higher the force that must be being applied to it. As I pointed out, in our biomechanics assessments we do not know where that force is coming from: it may be internal, it may external or a combination of both. I think EMG might be of some use here to attempt to differentiate, but this has it's limitations too, since EMG doesn't measure muscle force.

To make things more complicated the tissues are visco-elastic. This means that their stress/ strain characteristics are dependent upon the rate of loading. When a load is applied more rapidly, the slope of the tissues stress/ strain curves are seen to increase. Thus the tissues will become stiffer the faster they are loaded.

The area beneath the stress/ strain curve = the energy stored, so the strain rate would appear to have the capacity to influence this factor too in visco-elastic tissues. There is a limit as to how much energy we can try to store in a tissue. The way I have always thought about this is if we inflate a balloon, we are storing elastic strain energy in the skin of the balloon. If we keep putting more air into the balloon we store more energy in it's skin, but any child realises that there is a limit here!

So the question becomes is it better in terms of injury prevention to load a tissue rapidly or slowly? There have been several studies looking at the velocity of pronation, but the results often seem contradictory. Messier SP, Pittala KA. Etiologic factors associated with selected running injuries. Med Sci Sports Exerc. 1988;20:501-505 reported higher pronation velocity and excursion in injured runners with MTSS compared to non-injured runners, but no difference between runners with anterior knee pain and the uninjured group. While Hreljac A, Marshall RN, Hume PA. Evaluation of lower extremity overuse injury potential in runners. Med Sci Sports Exerc. 2000;32:1635-1641 reported that runners who had never had an overuse injury exhibited greater pronation velocity than runners who had sustained an overuse injury. So the jury seems to be out on that one.

Momentum = mass x velocity. The above studies reported velocity; this is not necessarilly the same thing when we are thinking about the rate of change of momentum and the "braking" forces. Without pulling the studies above, and looking at their data I'm not sure what the rate of change of velocity was. Yet the higher pronation velocity and greater excursion in the MTSS group of Messier, suggests "lower braking forces" in the injured group. However, momentum = mass x velocity and while the segmental masses are constant within each individual, they are not constant across a population.

N.B. without knowing the segmental masses of each individual, we cannot really identify the rate of change of momentum by looking at rate of change in velocity in isolation. Thus we should be cautious in comparing segmental velocities across a population and making inferences to the rate of change of momentum, i.e the forces at play. Since the same rate of change of velocity in body segments of different masses does not equate to the same rate of change of momentum.

The above studies do suggest that the velocity of the same body segment may be important in some pathologies but not in others though. Which brings me back to the normative database... I'll save that for later.

We may have to agree to disagree on this one. You can't say what is happening to the joint moments with the data at your disposal here, which is what I was trying to point out in my previous posts.

Ultimately thats what we all, quite rightly come back to- the change in subjective symptoms!

I think we need to be clear here that while Kevin's paper on the subtalar joint axis location and rotational equilibrium (SALRE) theory and the tissue stress approach to patient management are intertwined, they are not the same thing. So when you ask "what SALRE approach do you take for hip and pelvis pain", that doesn't really make a lot of sense to me. Applying tissue stress theory we should use the same approach to hip and pelvic pain as any other location of pain within the body, I'll quote Kevin here to save time as I have to head off to work soon:

"How Tissue Stress Theory Can Guide Orthotic Prescriptions
With these facts of tissue biomechanics in mind, incorporating tissue stress theory into the design of prescription foot orthosis therapy should enable injured tissues to resume function within the elastic region of their stress-strain curve, reducing the risk of further tissue injury and allowing more prompt tissue healing to occur. The three goals of prescription foot orthosis therapy using tissue stress theory are: reducing the pathological loading forces on the injured structural components of the foot and lower extremity; optimizing overall gait function; and preventing other pathologies from occurring.13,15

In the clinical setting, the podiatrist using tissue stress theory needs to utilize the following steps in order to optimize prescription foot orthosis therapy.13,15

First, specifically identify the anatomical structure that is the source of the patient?s complaints. This requires the podiatrist to have a detailed understanding of foot and lower extremity anatomy, a good understanding of clinical tests and access to diagnostic studies that can help identify which structural component is injured.

Second, the podiatrist needs to determine the structural and/or functional variables that may be the source of the pathological forces acting on the injured structure. A complete history, biomechanical examination of the foot and lower extremity, muscle testing, range of motion examination, and gait evaluation may all be necessary to determine what structural and/or functional variables are the main cause or causes of the excessive stress on the injured anatomical structure.

Finally, formulate a therapeutic treatment plan, including specific foot orthosis modifications, shoe modifications, bracing, stretching, strengthening, physical therapy modalities, injection therapy and surgery. One should carry out this plan in a logical sequence in order to optimize patient healing.

Using tissue stress theory to optimize foot orthosis design for patients with mechanically-based foot and lower extremity pathologies requires podiatrists to have a good appreciation of which anatomical structures are subject to tension, compression and shearing stresses during weightbearing activities. In addition, podiatrists must also understand the various ways that they may alter the design of foot orthoses to lessen the magnitude of abnormal stresses acting within the injured tissues of the foot and lower extremity. In other words, the podiatrist must have a good comprehension of the many variables that may mechanically affect the internal loading forces acting on the external and internal structural components of the foot and lower extremity during weightbearing activities.15"

- See more at: http://www.podiatrytoday.com/prescr...y-supplanted-root-theory#sthash.NU1hC9Z0.dpuf

Good discussion.

 

:good: Best post on Podiatry Arena for 2016, Dr. Spooner. Excellent!!

 

Simon - I like your thinking in terms of 'force = change in momentum" I never really think of it that way. However in this case Simon since these changes you speak of are in angular velocities then we should consider the term - torque (moments) = change in angular momentum.
So if angular momentum = inertial moment (I) * angular velocity (w) and so there is an inversely proportional change between I&w while the angular momentum remains the same. So if the Inertial moment or radius of gyration was changed or different between two segments but the mass was constant the angular velocity would change respectively. If therefore the angular momentum remains constant the applied torque or moment must still be constant and so the applied force about the moment arm would remain constant.

I think I've got that right, I haven't thought about these things in this way for quite a while.

Cheers Dave

PS yes like a dancer getting faster in a spin by retracting the arms and legs to make the radius of gyration shorter with respect to the axis of rotation. = conservation of angular momentum

 

Anyway to get back to the OP and replying to Eric and Trevor. I got the guy back today and there were no muscle weaknesses or imbalance including peroneals. I tried temp medial and lateral posting but there was no discernible visual kinematic change with either except a tendency to greater toe out with the lateral wedging. However he reported the lateral posting felt more comfortable.

Dave

 

Agreed

 

Thanks for the update. Interestingly, my observations with limited internal hip rotation, or rather an external hip position is that generally, if a patient has a relatively straight angle of gait, they will have more of what we would term a supinated foot type.

By contrast, if they have a lower arch, more pronated foot type, they tend to have a more abducted angle of gait.

It is interesting that increasing pronation moments abducted the foot. I wonder what effect that may have on the ankle, knee and hip.

 

I think we need to be clear here that while Kevin's paper on the subtalar joint axis location and rotational equilibrium (SALRE) theory and the tissue stress approach to patient management are intertwined, they are not the same thing. So when you ask "what SALRE approach do you take for hip and pelvis pain", that doesn't really make a lot of sense to me. Applying tissue stress theory we should use the same approach to hip and pelvic pain as any other location of pain within the body, I'll quote Kevin here to save time as I have to head off to work soon:]

Just to clarify, I was trying to suggest they were one of the same thing (although the subsequent quote was well written and a very good explanation). It was more about how SALRE is used to reduce tissue stress more proximally. I threw that out a little as it could potentially start a whole new thread. Plenty has been written regarding tib post, peroneals, lateral ankle etc. Much less on proximal issues. How do you determine at the hip whteher the altered function is hip adduction, rotation or contra-lateral pelvic drop as this would need to be known in order to try and reduce stress. Similarly, patella tendonopathy does not fall as easily into a pronation / supination moment model.

I am genuinely interested in how others apply the SALRE concepts to the provision of orthoses for proximal complaints.

One final comment, we will agree to disagree on some of the issues we have discussed but suffice is to say, the approach I take tries to indivdualise the management of patients but uses the normal ranges to try and give me some objectivity. There are limitations as there are when we use no tools and, whilst you may feel these flaws limit the interpretations, it does not mean the approach has no merit. Essentially you, me, anyone does not know. In others words, whilst you may not feel it is right, you cannot say it is wrong, as always, further research is required. That we can discuss over a beer at Summer School.

Not sure what I did wrong when I tried to post this the first time.

 

Trevor,
To understand how one could apply SALRE to proximal complaints one needs to understand how we apply SALRE to foot complaints. This is the tissue stress approach. Let's say we have a foot we have determined has peroneal tendonitis from overload of the peroneal muscles. We use SALRE to look at why the peroneal muscles are overloaded. A supination moment from ground reaction force would be trying to invert the STJ, the person feels this as unstable and uses their peroneal muscles to reduce that instability. SALRE tells us that there will be smaller demand for peroneal muscle activity if there is a greater pronation moment from the ground. So, if we shift the center of pressure under the foot more laterally there will be a greater pronation moment from the ground. This is how we determine what the treatment should be with SALRE. We are not comparing anything to a population average we are modeling how to reduce stress on a specific injured structure.

So, how can we use SALRE to treat more proximal structures? We would have to model those proximal structures and figure out how STJ pronation or supination moments will alter stress on those structures. You can certainly make the case that STJ moments will affect lower leg internal and external rotation moments. When you look at joint power studies, there is only a small portion of the time (immediately after heel contact) when ground reaction force is driving leg rotation. The majority of the time the power flows from the leg into the foot (That is the leg is driving the motion [could be muscle could be body momentum.]) One of the major treatment modality with SALRE is to shift the location of force under the foot. For structures higher up than the lower leg muscles SALRE is going to have a very small impact.

On the other hand, you can still identify injured structures anywhere in the body and then model them to figure out what interventions/behavior changes can lower the stress on those injured structures. Again, you can do that without knowing what average or normal is. You just have to know what will lower stress in the structure that you care about.

Eric

 

Further to Eric's reply. I think you picked a great example here with patella tendinopathy, Trevor.

Ignoring the "subtalar joint axis location" bit of SALRE, replacing it with Knee joint axis location and then focusing on the "rotational equilibrium" bit, it seems reasonable to assume that patella tendon loading is influenced by several variables, including the patellar tendon moment arm, the knee flexion angle, and the knee extensor moment generated during the landing action during either running (or more commonly with this pathology) jumping.

In order to think about the patella tendon moment arm we really need to employ a sagittal plane model in the first instance. From this it is clear that if the net GRF vector passes posterior to the knee joint axis in this model then the net external knee joint moment should be that of flexion which will increase the loading acting on the patella tendon. From the literature it seems that the peak patella tendon moment arm occurs between 45 and 60 degrees of knee flexion.

So, how do we use rotational equilibrium theory here to our advantage? Well in the short term at least, we probably need to reduce the magnitude of the knee flexion moment during "landing" either during jumping or running to reduce the stress on the patella tendon- how can we do that? We can either reduce the magnitude of the net GRF vector, or we can reduce its lever arm relative to the knee joint axis or we can provide an alternative source of knee joint extension moment. Or, all of the afore mentioned.

We could try by promoting a landing pattern which results in less knee flexion, this could result in a decrease in the net GRF vector lever arm. How might we achieve this? Increase hamstring length, more compliant surface, change in landing pattern etc. It might also be possible to achieve this via decreased posterior heel flare, reduced "drop", decoupled heel on footwear, negative heel etc.

As a progression to our treatment plan ultimately we want to try to increase the strength of the quads/ patella tendon themselves so that they are better able to resist the moment being applied to them- this is where progressive loading comes in.

I should be interested to hear of anyone's particular successes with this condition employing specific orthoses modifications other than increasing surface compliance, rounded inferior surface to the heel cup, i.e. no external rearfoot posting "block, as I'm yet to really find the key to orthosis design for this condition myself. Just thinking out-loud, perhaps a top-cover with decreased co-efficient of friction might be useful here to allow some forward translation of the foot, as this should result in a decrease in the posterior angulation of the net GRF during initial contact.... Maybe create a negative heel orthosis such that the forefoot extension is thicker than the shell material beneath the heel = increase gastrocnemius tension = increased internal knee extension moment from a source other than the patella tendon.... watch your Achilles though!

So, back to your original question with further interpretaion, Trevor... How does the subtalar joint axis location influence the knee joint extension/ flexion moments during loading response? That is the question we need to ask here. I'm not sure it does... But if we apply tissue stress and rotational equilibrium theories we realise that our therapies, including our foot orthoses (if designed with the right features), should be capable of altering moments about the knee joint axis too- right? Which is what we call the "tissue stress approach".

So, for those following along here, you see what I am trying to come up with? The tissue stress approach=

1) Identify the tissue under adverse stress. That was easy since Trevor told me it was a Patella Tendinopathy.
2) What is the function of the patella tendon? It's primary function is to supply internal knee extension moment from the quadriceps about the knee joint axis (it may have some role in resisting tibial-femoral- transverse plane rotation, but I focused upon it's primary role here).
3) Build a model, I did this in my head here, but we could draw it out, in this case I'd start by drawing a sagittal plane model. But maybe go to to transverse and frontal for a more complete analysis.
4) In order to reduce stress on the tissue we need to: a) reduce external knee flexion moment and/ or b) increase knee extension moment from a different source.
5) Design a treatment plan to achieve 3) above. There will be many ways of skinning the cat here- the key is in not inducing pathology elsewhere. "And that's the real trick"- Han Solo- despite technology, the only way to judge this is via subjective symptoms- hence my previous posts in this thread, end of story

Don't need the mean of a data set, nor an idea of "normal function" to achieve that, just need to look at the individual in front of me. Since, Phenotype = Genotype + Environment + (Genotype x Environment) + measurement error = everyone is a case study of just one.

 

Keep dipping back into this discussion (and having to re-read chunks to get my head around some of it). Thanks for it, enjoyable and not quite drowning, yet.

 

Simon wrote

And these externally applied moments might include devices like GRAFO KAFO or flexion limiting knee brace or a walking stick. While these might not appeal to the sportsman they do effectively reduce internal forces and extension moments required to resist knee flexion.

Dave Smith

 

Agreed

 

I have enjoyed reading the responses of Simon and Eric to Trevor's question regarding Tissue Stress Theory and Subtalar Joint Axis Location and Rotational Equilibrium (SALRE) Theory. Maybe I can clarify some things to make it easier for those following along.

SALRE Theory is not a theory of how one may treat every foot and lower extremity mechanical pathology. In fact, SALRE Theory is not really a theory that specifically deals with the treatment of foot pathologies.

What then is SALRE Theory? SALRE Theory is a theory which describes how the spatial location of the subtalar joint (STJ) axis determines the external STJ pronation and supination moments from ground reaction force (GRF) which, in turn, is important in determining the internal pronation and supination moments which help resist the STJ moments from GRF. SALRE Theory also provides the following coherent biomechanical explanations (to name a few):

1. Explains how the frontal plane shape and transverse plane shape of the foot segments may cause alterations in the external and internal STJ moments.
2. Explains how the major flatfoot surgeries of the rearfoot and midfoot mechanically alter STJ pronation/supination moments.
3. Explains how foot orthoses produce their mechanical actions on the STJ.
4. Explains why some feet are more hard to supinate with foot orthoses and why some feet are more easy to supinate and harder to pronate.
5. Explains how posterior tibial tendon dysfunction may occur over time in patients with preexisting flatfoot deformity.
6. Explains why sinus tarsi syndrome may occur and why anti-pronation foot orthoses may help relieve the pain from sinus tarsi syndrome.

On the other hand, Tissue Stress Theory, as Eric and Simon pointed out so well, is a treatment approach that targets the tissue (i.e. bone, ligament, fascia, tendon, muscle, cartilage or skin) that is injured and determines the best way to mechanically heal that tissue, without injuring other tissues.

Here is a segment from the book chapter on Tissue Stress Theory that Eric and I wrote back in 2004 and was finally published in 2013 (Fuller EA, Kirby KA: Subtalar joint equilibrium and tissue stress approach to biomechanical therapy of the foot and lower extremity. In Albert SF, Curran SA (eds): Biomechanics of the Lower Extremity: Theory and Practice, Volume 1. Bipedmed, LLC, Denver, 2013, pp. 205-264).

Therefore, you see, Tissue Stress Theory does not limit itself to SALRE Theory or to the actions of the STJ during gait. Rather, Tissue Stress Theory is a treatment method by which the attention of the clinician is focused more on the biomechanics of the injured tissue and less on the measurement of foot and lower extremity "deformities" and does not necessarily need in-shoe pressure analysis, 3D motion analysis, or pressure mat analysis to heal the patient's injury. What is needed from the clinician is an excellent understanding of foot and lower extremity anatomy, a good understanding of basic biomechanics and engineering principles and a good understanding of normal gait biomechanics and muscle function. All in all, Tissue Stress Theory does rely on the clinician's intimate knowledge of foot and lower extremity biomechanics that is gained from a full understanding of SALRE Theory to make the best mechanically-related treatment decisions for their patients.

Good discussion.:drinks

 

Eric and Simon already have mentioned the use of modeling techniques and how they are very important in understanding the use of tissue stress theory in the treatment of any mechanically related pathologies in the foot and lower extremity.

Modeling is based on the idea that simple mechanical representations of any part of the foot and lower extremity may be done with only a basic knowledge of whether tension or compression or torsional forces are acting across these these structural components of the foot and lower extremity. These models may be used to estimate not only how much force is going through this structural component but also may be used to estimate how orthoses, braces and other treatment techniques can be used to lessen the load on any structural components of the foot and lower extremity.

 

I think this dissonance experienced by many between understanding the difference between visual observation of motion and intuitively estimating the internal force is that muscle length and therefore joint range of motion is no indicator of force in the muscle unit of interest. So where increased range of motion during and action of interest might indicate increased external forces and therefore corresponding internal resisting forces it may be actually be the opposite. Also decreased RoM for the same action may indicate increased internal forces. The only way to no for sure is to be able to estimate the balance between internal and external moments, which as Kevin says requires knowledge of anatomy and mechanical principles and the application of both to reach a reasonable conclusion about internal forces in the tissue of interest - this is the underlying principle of SALRE. The (rotational) equilibrium of moments principle is equally valid in any condition where a force has a lever to tend to cause a rotation.
Then when you add in the complications of plastic deformation and the non Newtonian properties of all biological tissues there are problems of loading rate and time dependency but these are probably or usually much less significant than the principle of understanding and applying rotational equilibrium of moments.

Regards Dave