Does the Stance Leg Push or Does the Swing Leg Pull?

Hi Stanley,

Sorry about the article Stanley. My copy is in a box that hasn't been opened since moving. I will try and dig it out this weekend. It does not appear to be available online.

I don't understand why you think the Winter article is deficient. When joint moments are calculated with inverse dynamics, the net moment at a joint is found. When a muscle contracts it produces a force that creates a moment at a joint. This moment is what may or may not contribute to motion. So, there is more than one way to assess the contribution of a muscle to movement.

Incidentally, Winter has also written on using EMG to assess muscle force. I don't recall if there is a different EMG pattern/ magnitude for eccentric vs. concentric contractions. I do remember there were problems assessing muscle force with EMG. Once you know the muscle force, you still have to know the lever arm of the tendon at the joint to calculate moment. Then you have to look at velocity and accelerations to see if the force is limiting motion or causing motion.

Energy stored in the tendon would contribute to joint power and would be included in joint power calculations. So, given the question is whether or not ankle push adds energy to swing leg prior to toe off, you could use EMG with some other data, or you could look at joint power to answer the question. As Kevin pointed out there is time lag in force produced versus the EMG. That is there is EMG activity before force is produced and there is muscle force produced for a period of time after the EMG has stopped.

Just before toe off, before the swing leg becomes the swing leg, ankle plantar flexion may provide energy to the swing leg. So, yes you could say that swing leg provided energy for forward propulsion, but you would be confusing the issue because the energy was generated before it became the swing leg.

If you had a force, with a magnitude of 50 Newtons, described by a vector that had an angle of 36degrees to the floor, the magnitude of the horizontal component would be 50*cos(36) and the vertical component would be 50*sin(36).

You need to add the experimental condition to the conclusion.... when a string is attached to your leg on a treadmill. I need to reread the article and see if they looked to see how much different the EMG should be to reach their conclusion.

I still don't see how you get knee extension. We are talking about the trailing during the end of double support. With this geometry, I agree ankle plantar flexion will cause the lower end of the leg to move faster. If the hip velocity increases less than the lower leg velocity then the lower leg will get closer to the hip and knee flexion has to occur.

Regards,

Eric

 

From the article

EMG. We reject the hypothesis that activation of ankle
plantar flexors would decrease with ESA. We did not find
changes in mEMG of the MG and Sol muscles with ESA in the
second half of stance phase. These results suggest that the
plantar flexor muscle group is not responsible for leg swing
initiation in running. This finding is in contrast to the idea
raised in several walking studies that the ankle plantar flexor(s)
initiate leg swing (16, 23, 26). We attribute the activation of the
ankle plantar flexor muscles in late stance to the functions of
forward propulsion and supporting body weight.​

The problem with the conclusion is that they don't examine how much of the plantar flexion contraction and EMG goes to actual plantar flexion versus just supporting body weight. They found that there was not a significant decrease in EMG with the string pulling their foot forward. They did not address whether the difference between push plus body weight versus just body weight was measurable. Just before toe off, the heel is off of the ground and a large activity of the muscle is required just to hold the ankle in the same position against the dorsiflexion force from ground reaction force. The additional effort to move the leg forward may be very small compared to the effort just to hold foot in the same position.

Then they attribute the activiation of the plantar flexors to the function of forward propulsion and supporting of body weight. The supporting of body weight is going to be a lot of the force. Forward propulsion is the same thing as initiating swing the force to do both is the same.

Regards,

Eric

 

I’ll be looking forward to it. I hope you like your new place.

First of all, I can’t comment on something I haven’t read. In my last post I quoted other writers who found it deficient, if this is the article you are referring to. According to you, using inverse dynamics gives you the net moment. So it doesn’t tell you exactly which muscles are contributing and how much each muscle is contributing to the moment around a joint. It doesn’t tell you if the work is being done by a concentric contraction or stored energy.

It would be nice if I saw the study you are referring to.

I agree that the energy stored would be included in joint power calculations. That is why Winter (from what I have ascertained from you and other writers) does not tell what is contributing to the moment. The study by Modica is a straight forward article that shows that the plantar flexors do not initiate swing.

You said may. Since the Modica paper shows it wasn’t from the contraction of the gastrocnemius muscle, in normal running, so you are probably dealing with abnormal gait, and referring to it as possibly normal.

I agree Eric, we should add the experimental condition to the conclusion. I don’t know the Winter article, so it is impossible for me to add the experimental conditions to it and curiously, you haven’t added any experimental conditions to it. As far as the Neptune article, the experimental condition was on a model with a limited number of actuators and no subtalar joint. I think that using a string to assist the swing leg in a live human is a better model to work from.

At the end of double support the foot would be the most vertical to the ground. Assume for a moment that the foot would be perpendicular to the ground. The ankle would be force to move in a horizontal manner. If the ankle is proceeding quicker than the knee, then the tibia would be forced into a position that extends the knee. I made a quick stick figure on Paint to illustrate the point. (See below)

Eric, what they found was if swing was assisted there was no change in plantar flexor contraction. What we can say from this is that muscle contraction of the plantar flexors does not initiate swing. Every other conclusion is conjecture. So we have to go with a theory that explains everything. Winter (according to you) shows there are moments from the ankle flexors that power push off and swing (If I am misquoting you, then please correct me). Modica shows that the plantarflexors do not fire. There is only one way to reconcile this, and that is to say that the moments that Winter sees is not from active muscle contraction of the plantarflexors, but rather from stored energy of the tendons and other soft tissue structures.

Regards,

Stanley

 

Hi Stanley,

I agree that the power calculations don't parse out which of many possible muscles contribute to joint motion. What they do show is whether or not a moment is there. If there is a plantar flexion moment and ankle joint plantar flexion motion then an ankle plantar flexion muscle created that motion. You can't get around Newton's second law for angular motion. Moment = moment of inertia x angular acceleration.

I said that that the ankle plantar flexors may push the leg forward. The "may" qualifier is added because of Winter's paper that showed that there is a trade off between ankle push and hip pull. When there is ankle push, hip pull is not needed. When there is no ankle push hip pull is needed to initiate swing.

Have you ever seen Howard Dannenberg's Hallux Limitus lecture where he has before and after orthotic video. Before there is no ankle plantar flexion and hence no ankle power. After there is ankle plantar flexion. I certainly thought that the after gait was more normal. Stanley, what are your criteria for normal gait and why do you think that those criteria should be used?

Stanley, have you already decided that the Modica paper is a better model to work from without having read Winter's papers on the subject? David Winter is highly respected past president of the international society of biomechanics and has been keynote speaker at their conferences.

This is a great picture for showing how ankle plantar flexion can cause hip flexion and add power to the soon to be swing leg. Yes, posterior to anterior shear force from the ground acting on the foot will tend to cause knee extension. It will also tend to cause hip flexion. So how do we decide whether we get knee extension or hip flexion? Well we can look at joint powers. Or we can look at what happens and what is possible. If you were walking and you tried to swing your leg forward and it extened at the knee you would stub your toe and trip. To avoid this you could increase activity of the knee flexion muscles which would increase stiffness of he knee and the push form the ankle would not extend the knee, but flex the hip. This is the ankle push that I have been talking about.

I had the pleasure of reading Winter's work before watching my children learn how to walk. When you learn to walk you make the mistake of extending your knee when you should flex and you fall down. Gait is not hard wired, but learned. I question the notion that there is a normal gait. There are many different ways to achieve the same motion.

What the Modica article showed was that there was not a measurable change in EMG when running with and without the string attached to pull the foot forward. The problems with this include that the subjects may have been running without ankle plantarflexion power without the pull. We know it is possible to move without ankle push, but that does not mean it is not possible to run with ankle push. Another problem is that they did not address whether or not the EMG would change enough with and without the string attached to be significant with respect to the measurement error of EMG. There are many problems with force estimates from EMG.

I again want to reiterate that there is a trade off between ankle push and hip pull. If you don't use one, you have to use the other. I am not saying that ankle push happens every step in every person. I am saying that is possible and when it does occur it looks like a gait that is more desirable than without.

Regards,

Eric Fuller

 

Hi Eric,

I hope you are enjoying your new house.

I’m glad we agree.

Normal is a term that is used differently by different people. There is average normal (What normal people have i.e. death, dental caries, etc.) There is ideal that is considered normal (dorsiflexion 10 degrees) and there is normal for that individual, which is what I think you are referring to. Normal gait with this definition would be the most efficient way for the person to move, and one that doesn’t cause pain (as in taking too long a stride). This gait does not require conscious effort.
Regarding Howard’s lecture, what you are seeing (and Howard correct me if I am wrong, as it is your work) is the blockage of sagittal plane motion prevents the storing of energy in the Achilles tendon and associated soft tissue structures.

How can I decide when I haven’t seen the article?
So I take it that there are no experimental conditions to the Winter article.

Eric, according to you quoting Winter: When there is ankle push, hip pull is not needed. When there is no ankle push hip pull is needed to initiate swing, So isn’t it contradictory to say that ankle push could cause hip flexion?

Unfortunately, I haven’t had the pleasure of reading Winter’s work. It must be an incredible article to discuss how children have no hard wiring in learning to walk. Could you tell me how he explains the amphibian crawling, the reptilian crawling, and the gorilloid walking with the hands over the head?

Thanks for making me reread the article in greater depth. It is a rather well written article.
Actually the Modica article showed that there was not a measurable change in EMG when running with and without the external swing assist (ESA) device only in certain muscles.

Eric, If you are saying that the subjects may have been running without ankle plantarflexion power and without the pull, then how did they run? If you are saying that if the hip pull was powering swing in these subjects, then the ESA would not cause a change in the plantar flexor EMG’s as seen in this study. That’s true Eric, but how can you explain the change in the Rectus Femoris EMG?

The article clearly says
“Overview. Subjects ran on a motor driven treadmill normally and with anterior pulling forces applied to their feet during late stance and early swing phases. We measured metabolic energy expenditure, stride kinematics, and surface EMG signals of selected leg muscles.” It continues with
“Protocol. The experiment commenced with a standing metabolic rate trial and a 10-min control (normal running) trial without the external swing assist (ESA 0%).”
So Eric, there is a control with no ESA (ESA 0%).
Furthermore Figure 5 shows an almost linear change with the amount of extrnal swing assist force starting with ESA of 0%BW.

The study did not use force estimates, only percentages of the normal running leg. Curiously,
“before the experiment, subjects performed a series of contractions to ensure cross talk was negligible”
as per a Winter article.

I would like to reiterate that we have to go with a theory that explains everything. Winter (according to you) shows there are moments from the ankle flexors that power push off and swing (If I am misquoting you, then please correct me). Modica shows that the plantarflexors do not fire. There is only one way to reconcile this, and that is to say that the moments that Winter sees is not from active muscle contraction of the plantarflexors, but rather from stored energy of the tendons and other soft tissue structures.

Regards,

Stanley

 

Hi Stanley,

Great discussion

Actually, it wasn't a move to new house. It was from packing up an office when I left CCPM.

Howard's explanation is one explanation of the phenomenon of more efficient gait after orthotics. I disagree with his explanation and that is what the title of this thread is about. Actually, Howard has said that its not possible to have ankle push. He has said the spinal engine is where the power for the swing leg comes from. He has said that the sagittal blockade prevents hip extension and that is where the elastic energy is stored and then later provided to the swing leg. (Howard, correct me if I'm wrong and tell me if this is what you still believe.)

The Winter articles (and there are many) show that ankle push does occur and that is one reason why I disagree with Howard's explanation. Other reasons include: Elastic energy is not 100% efficient so you just don't get more flexion when you get more extension. The center of mass is very high relative to the point of "blockade" and it therefore can't really stop forward progression.

An alternate explanation is that there is a pain avoidance mechanism in gait that causes the sagittal plane blockade. The functional hallux limitus doesn't mechanically block forward progression. It hurts to have to try to stop gait with the blocked motion at the MPJ. A lot of people with functional hallux limitus will have hyperextension of the IPJ which at some point probably hurt. So, to avoid pain, the brain gives signals to the body to walk with a less propulsive gait. When the orthotics increase the available dorsiflexion of the hallux (Howard's very important and in my opinion true observation) the body relearns to walk with a propulsive gait which is more ideal in terms of energy consumption.

There can be more than one explanation for an observation.

The Winter paper (one of many) that I quote when I discuss the trade off between hip joint power and ankle power is a descriptive paper. There is no control. Many subjects were observed and had their joint powers measured, some on different days. He saw, in those measurements, an inverse correlation between hip power and ankle power. He also so variability across people and within people on different days. The conclusion from these observations is that people can use different strategies to add energy to the swing leg. In terms of Howard's observation you could use pain to explain why one strategy is chosen over another.

No. I see where you are confused by my terminology. Ankle push can be up and it can be forward. Specifically, with adequate friction, ankle push will cause a posterior to anterior force from the ground acting on the foot. This will cause hip flexion. You don't get ankle push on ice.

I'm sorry to have mislead you. Winter did not say that there was no hard wiring. It was my observations related to his work. In living, more is needed than straight ahead walking. We need to make right turns, jump, walk backwards amongst other things. If we were hard wired to walk straight ahead how are we able to do these other things? Also, if we were hard wired, why don't children walk the minute they are born? Learning occurs when human children begin to walk.

Agreed.

I didn't say that they could run without both hip pull and ankle push. They have to use one or the other and they may use both in running. (The data that I have been quoting has been on walking. I don't recall if running was addressed.) On my high school rowing team there was a guy we used to make fun of because his heel never lifted off of the ground when he ran. He often beat me on trail runs. So, it is possible to run relatively fast without ankle push.

The idea that there is less hip pull with the ESA is consistent with what I have been saying. There is less need for muscle power to swing the leg forward with the ESA (string attached to foot pulling it forward) There is some very good data in the Modica article. They were worried about injury when the ESA had >6% body weight. It takes very little force to swing the leg forward.

I agree there is a control, but they do not address whether or not a change in EMG could be seen with their protocol. At the time just before toe off there usually is heel lift. The heel lift could occur with or with out plantar flexion of the ankle because of the forward progression of the tibia. When the heel lift occurs a substantial portion of the gastroc and soleus force and hence EMG output would go to holding the ankle at the same angle against body weight. They did not address the question of how much more EMG activity is needed to cause plantar flexion. From their data, less than 6% of body weight is needed to swing the leg forward. At push off in running there is upward acceleration so the muscle is resisting greater than body weight. Is a <6% change within their measurement error.

After thinking about this some more, I have an additional problem related to the string attached to the foot. We know that there is a reduction in hip flexion musculature from their data with the string attached. How does the subject lift the soon to be swing leg off of the ground with reduced hip extensor activity? The leg has to be lifted to prevent tripping. Perhaps ankle plantar flexion was required to provide a vertical lift to allow the ESA to pull the swing leg forward. The experimental set up does not allow for the conclusion that ankle plantar flexion does not power leg swing. The string attached to the foot may alter gait in a way that you would not see a difference in EMG activity.

It would be interesting to joint power measurements on the experimental set up to see if there was a change in joint power. It would also be interesting to see what would happen if there was a change in the ankle of pull with the ESA so that there would be more leg lift.

The problem with their logic is that they assume that the EMG change would pick up a very small change in force.

Stanley, the Modica article showed that the plantar flexors were firing. The question is whether or not they were just supporting body weight or providing additional push. As I describe above, I don't think that they can make the conclusion about ankle plantar flexors from their experimental design. Another way to reconcile this is to admit the flaws in the Modica article and look at the other research that shows that there is ankle push to initiate swing leg motion.

There is a difference between a gait with ankle plantar flexion just before toe off and a gait with no ankle motion before toe off. Muscle is composed of the contractile element and the tendon element. The elastic element is passive and will be present and stretched whether or not there is ankle plantar flexion, in a gait with heel lift. The muscle unit is the difference between these two situations. Regardlass the muscle is producing a moment in both situations. There is a little more moment when there is ankle plantar flexion. I don't think that the elastic element of muscle resolves are disagreement.

Stanley, I'm not saying that ankle plantar flexion powers swing 100% of the time. I'm saying that occurs some of the time. Do you think that is theoretically possible?

Regards,

Eric

 

Eric,

You wrote "Howard's explanation is one explanation of the phenomenon of more efficient gait after orthotics. I disagree with his explanation and that is what the title of this thread is about. Actually, Howard has said that its not possible to have ankle push. He has said the spinal engine is where the power for the swing leg comes from. He has said that the sagittal blockade prevents hip extension and that is where the elastic energy is stored and then later provided to the swing leg. (Howard, correct me if I'm wrong and tell me if this is what you still believe.)"

For the last time...this is what I have ALWAYS said. At the time that the ankle "push" occurs, the limb is entering pre-swing phase. During this phase, the knee and hip begin rapid flexion. The rapid plantarflexion of the ankle directs it power to the swing limb, not to the CoM. Concurrent with ankle plantarflexion, the spinal engine is creating a forward directed pelvic rotation to the swing side, thus adding to the energy required for swing phase.

Now, in order for pre-swing phase to effectively be pre-loaded, extension of the hip joint during single support phase must occur. This is a direct function of the ability of the foot to permit sagittal plane motion. If this pre-load fails, then hip pull off (as you have noted Winter has described) becomes the default method of swing initiation. Other assist mechanisms such as lateral trunk bending also may occur, and these both can lead to overuse of the musculature of the lower back.

My issues with your and Kevin's explanations involves the power segment during single, not double support phase. The reactive longitudinal thrust curve becomes positive in midstep. Of this there is no argument. If eccentric contraction is occurring in the triceps surae during this period, and the gluteals have long since shut off, what is left to extend the hip (and entire lower limb) DURING SINGLE SUPPORT PHASE other than the swing limb and its combined affect with gravity on the CoM?

For as long as we have had these discussions, I am amazed that the timing between single and double support phases (and their associated motions) have alluded you. The weight bearing limb only extends during single support. At the moment the swing limb contacts the ground, the trailing limb immediately stops extending and reverses to flexion. This also times w/ the change in eccentric to contract triceps surae contraction. This is why I have been saying that the "ankle push" is not directed to the CoM...but rather to create an effective (and efficient) swing phase.

I never mind being quoted....just please do it correctly.

Best,
Howard

 

Howard:

I also don't like being misquoted.

Here is what I have said in the past and am saying currently regarding this discussion:

1. The swing phase limb cannot, by itself, without the pushing force from (see definition of "push" below) the stance phase limb on the ground, power the forward movement of walking gait. (See my previous mechanical analyses of "walking on ice" or "walking in space" or "walking during midflight on a trampoline" for further mechanical background using this logic.)

2. The swing phase limb, and its inherent mechanics, is a critical part of human walking and works in conjunction with the stance phase limb to allow optimum efficiency of gait.

3. Active concentric ankle joint plantarflexion occurs propulsion during normal walking that not only adds energy to the swing phase limb but also helps push the body forward (Neptune RR, Kautz SA, Zajac FE: Contributions of the individual ankle plantar flexors to support, forward progression and swing initiation during walking. Journal of Biomechanics, 34:11 : 1387-1398, 2001).

4. Even though the knee is flexing during propulsion, active posteriorly-directed pushing force is exerted from the foot to the ground (Zmitrewicz, R.J., Neptune, R.R., Walden, J.G., Rogers, W., and Bosker, G. (2006). The effect of foot-ankle prosthetic components on braking and propulsive impulses during transtibial amputee gait. Archives of Physical Medicine and Rehabilitation 87(10): 1334-1339). See graph below on the normal limb from the above paper by Zmitrewicz et al which nicely demonstrates this.

5. The analogy of "pushing a rope" to imply that the foot and lower extremity someow can't possibly exert a pushing force on the ground during propulsion is an improper analogy. The foot and lower extremity is not a continuously flexible object that cannot develop sufficient internal forces (i.e. compression and tension stresses) within its structure so that it cannot exert multiple types of pushing forces with the ground. Rather, the foot and lower extremity are more accurately modelled as four main rigid body segments, pelvis, thigh, shank and foot connected by three main articulations at the hip, knee and ankle that allow the individual nearly limitless methods of exerting all types of pushing forces on the ground during weightbearing activities.

Have a nice weekend.

 

Kevin,

Thanks for the detailed reply. As far as #5 above, I would like to ask a sincere question.

Please explain to me how, when the knee and hip are flexing, that plantarflexion of the ankle provides a forward directed moment to the CoM. For the life of me...I can't see how that can happen, particularly in light of the simultaneous braking created by heel contact on the contralateral side.

Also, when looking at the GRF graph, there is a point in mid step where braking changes to thrusting. How does this occur if the gluteals are turned off, and the triceps surae are still eccentrically contracting?

I absolutely agree that the power for gait is a complex issue. It is achieving max efficiency that makes the swing limb so attractive as a primary (yet not only) method for propulsion. And, not only does it work in the forward direction, but is omnidirectional, ie, forwards, backwards, left and right. Step in the direction you want to move, and the use the weight bearing limb to "passively" thrust the ground in the opposite direction. It is this omnidirectional component which I also find most intriguing, and fits well with efficiency as a primary goal of the development of human gait.

Howard

 

As we have said before, and I believed that you agreed that ankle plantar flexion adds energy to the swing leg just before toe off and not directly to the center of mass. At the end of swing this leg energy is transmitted to the body as the body slows the swing leg down before heel strike. So, ankle plantar flexion did not directly move the center of mass, but its action accelerates the center of mass indirectly.

Momentum of the body moves the body over the stance leg. When the center of mass is posterior to the center of pressure under the foot and there is a force couple on the body from ground reaction force causing a rearward rotational moment. This moment decelerates the forward progression of the body. It also is the cause of the ground reaction shear. Two situations, you lean backward enough so that your center of mass is behind your foot. Situation 1 is on ground with a high frictional coefficient. Situation 2 is on ice. In situation on the force couple of ground reaction force will cause you to rotate backward with the pivot point at your foot and you will land on your ass behind the point where you originally started. In situation 2 you will land on your ass at the same point you started, because there is no friction on the ground to hold the pivot point stationary. In situation 2 the inertia of the body holds the center of mass in the same position and there is no horizontal force to cause a horzontal acceleration of the center of mass. In situation one there is ground reactive shear that causes a posterior acceleration of the center of mass.

This is how you can see a reversal of the ground reaction shear without any contraction of the gluteals. The above model would predict that the shear is greatest when the center of mass is farther from the center of pressure. It would also predict that direction of shear would change as the center of mass moves anterior to the center of pressure, which also what is seen.

Yes, the swing leg is a significant component of the center of mass. As it moves forward it will help change the location of the center of mass. So, I agree that the movement of the swing leg does affect ground reaction shear, but it is just an effect of the total center of mass.

I agree using the center of mass of the body is an efficient way of producing ground reaction thrust. However, we should not complicate the issue more than necessary. It is quite easily explained by examining the location of the center of mass relative to the center of pressure.

Regards,

Eric

 

Howard:

Having these discussions with you over the years has really opened my eyes to what you have been lecturing on and writing on over the years....and I thank you for that insight. I can't agree with you completely, but certainly our discussions have broadened my horizons. In addition, having Eric provide his knowledge on gait mechanics, joint powers, etc has given me a "fuller" understanding of how gait may be analyzed and discussed.

My answer to your question is that as long as the magnitude of posterior shearing force from the late stance phase foot exceeds the magnitude of anterior shearing force from the early stance phase foot, at any instant in time, then a net anteriorly directed thrust will occur on the center of mass of the body. The swing phase limb's role in increasing this posterior shearing force from the late stance phase foot is critical...normal gait could not occur without it.

Have a great Holiday Season!

 

Hi Eric,

I agree. The questions you give me make me think and learn, and that is what a good discussion is about. I hope I am returning the favor.
I am writing this after Howard’s reply. So I will defer to his wisdom on the questions he answered.

I haven’t seen the Winter articles so I have no opinion. After reading Howard’s reply, I wonder if Winter did a biomechanical exam? Did he see if the subjects had hallux limitus? I agree that elastic energy is not 100% efficient; I don’t understand why it would have to be. As far as forward progression, people with hallux limitus can still walk, just not as well.

Eric, so you are saying that in the past the person had some pain related to hallux limitus, and they started walking with a less propulsive gait. They still continue to walk with this apropulsive gait without any pain. Now, orthoses are put in this asymptomatic foot and the body decides to relearn to walk. What if I were to put orthoses in that didn’t correct the hallux limitus, how would the body know that these orthoses were going to fix the problem and walk normally?

So did Winter discuss ice in his article, and say that when you get ankle push you get increased hip flexion?

Eric, it is your contention that everything is learned. What is happening is that there is a development of the nervous system that mimics evolution that allows for different things to occur at different times. To say that everything is learned ignores the reality of the development of gait. I wonder how a child is supposed to learn to ignore his Babinski response at six months of age. When you figure that out, then I have hundreds of patients with CVA’s that require your services and a nomination for the Nobel prize in medicine.

Or relatively slow with ankle push. Did you check him for a hallux limitus?

but there was no change in muscle power of the medial gastroc and the soleus.

One very interesting fact in the Modica article is that he found the energetic cost of leg swing to be greater than 20% in running.

There is a change in the EMG of the rectus femoris.

Eric, earlier in our discussion Kevin said: “The foot during propulsion does not need to lift the full body weight vertically upward, it only needs to push the center of mass forward and accelerate the leg into swing.” So are you disagreeing with him?

If you read the article closely, it talked about the iliopsoas muscle that unfortunately wasn’t tested.

In fact the result showed that the muscles that cause ankle plantarflexion do not actively power leg swing. That is not to say that the tendons and other soft tissue structures do not contribute, as this was not tested. If you take the Winter article that says that there is ankle power contributing to leg swing (it does say this doesn’t it?) and subtract the fact that the muscles do not actively cause this to occur from the Modica article, then the difference is every other structure that can cause ankle plantarflexion, and that is the Achilles tendon, the fascia around the sarcomeres and the fascia.
Eric, if you look at the data, you will see a linear change depending on the % of body weight, which shows that the ESA did not affect gait other than assisiting swing. So let’s use your concepts to the Winter article you told me about (which I haven’t read yet). The people had a change in joint power from day to day, and from this you conclude that there are variable ways to power swing. If the person wears different shoes, or different clothes, then you could see a variation in gait. What if the pants were tight on one day, and looser on another day. So the article may just be measuring joint power against clothing. This is why there are controls in scientific papers.

I don’t understand your point. They saw significant changes in the rectus femoris with the ESA, and none with the soleus or medial gastrocnemius.

Eric, it seems the Modica article does not have any more flaws then the studies you are presenting. The only flaw that you really can come up with is that there is an ESA, and the linear data showed, outside of the force on the swing leg, there was no additional effect. The bottom line is that you start with runners that have leg swing, you measure the contraction of the plantar flexors, you aid the leg swing and you remeasure the contraction of the plantar flexors. The only logical explanation is to say that the plantar flexors are not involved in leg swing. The firing of the ankle plantar flexors is therefore doing something else. What the plantarflexors are doing is not answered by this study, only that it is not assisting in swing.

Eric, you are not factoring in where body weight is at the moment of heel off.
At heel off, body weight is over the 1st MPJ, so body is balanced at this point, and heel off requires no force. That is the passive plantarflexion you talk about. Any energy stored in the soft tissues will be released to help plantarflexion at this time.

The question is what powers ankle flexion?

Regards,

Stanley

 

Eric,

Did you really write "we should not complicate the issue more than necessary". Amazing!!!

That said....I do appreciate your explanations...and have learned a lot from them. This has been a terrific discussion.

So, you have written that momentum and the effect of the CoM relative to the CoP are significant methods of creating propulsion. I agree completely. And the way we move the CoM relative to the CoP efficiently is via the swing limb. Herman, etal, (Neural Control of Locomotion) have described that swing phase muscle activity is hard wired within the neural system. Pick up an infant by their arms, and they step. So the motion of the swing limb (provided neurological defect, ie CP, are not present) and its affect on the CoM (and ultimately the CoP) are predictably present with each step.

So, the real question is this. Since this couple does move the CoM, then what happens if the stance side foot fails to allow the sagittally directed movement at the time the CoM is being moved over the CoP?

This simple fact is that either storage or dissipation of this force must occur. Since storage is limited, dissipation becomes the path of least resistance. And, considering that the timing of this "dissipation event" must match the timing of the return kinetic energy in the 2nd half of single support phase...it will occur at the precise time we see "excessive midstance pronation".

So, the real point here is do we control the motion related to the pronation we see...or do we create a device which permits the sagittal plane motion to occur, and thus relieves the need to dissipate this force in a pathologic way.

Howard

 

Hi Stanley,

If orthoses did not correct the hallux limitus there would still be pain when someone tried to walk with a longer stride. If they did correct the hallux limitus then during various activities the individual would subconsciously notice that they could take longer strides without pain and then choose to walk with a more efficient gait.

I looked for my copies this weekend and couldn't find them. I don't recall if he addressed the amount of hip flexion.

I'm not saying that everything is learned. I don't remember why the babinski reflex goes away, so I can't say that is learned. In regards to the CVA patient, you need an intact brain to control the muscles so you cannot learn to move a muscle you cannot move. If you have an intact brain you learn to use the muscles to place the leg in the optimum location for efficient gait that avoids painful motions.

In the Modica article there was no measurable change in the EMG. Power from the muscles was not measured.

My quote was referring to running. In walking I would agree with what Kevin said.

Just before toe off in running, most of the time the heel is off of the ground. When the heel is off of the ground at this point in time the plantar flexors will be resisting a force greater than body weight. The Modica article showed that a force of greater than 6% of body weight caused muscle soreness from the muscles that slow the swing leg down before heel strike. So, it takes less than 6% of body weight to swing the leg forward. Can an EMG recording accurately measure a less than 6% change in force from the muscle?

The better argument against the conclusion reached is that there has to me some lift of the trailing leg to prevent tripping during swing. The hip flexors, which could provide some lift of the swing leg are used less in the presence of the ESA. So, you may need more ankle plantar flexor activity to get an upward push.

The ankle plantar flexors are active because they need to support body body weight when the heel lifts off of the ground.

The timing of heel lift is variable across people.

When heel lift occurs there may or may not be ankle plantar flexion. The forward rotation of the tibia can cause heel lift without ankle plantar flexion. However, when heel off occurs there are forces involved. When the heel lifts, the center of pressure of ground reaction force will be anterior to the ankle joint and will be causing a dorsiflexion moment at the ankle joint. For the joint to remain stationary, there must be an equal and opposite plantar flexion moment from something at the ankle joint. The most likely candidate is from the Achilles tendon. You could get an ankle plantar flexion moment from contact forces of the talus on the anterior aspect of the tibia, but this would quickly become painful. Beyond the plantaris tendon there are not really any any anatomical structures beyond these that could produce significant plantar flexion moment to resist the considerable dorsiflexion moment from the ground.

Regards,

Eric

 

Hi Howard,

I am glad that we are in agreement about CoM and Cop. Hardwiring of gait happens to a point and is probably at the level of reflexes. However, it cannot be entirely hard wired. We have to be able to go up and down stairs, make left turns and walk on uneven terrain. The reflexes have to be overridden to be able to move in the real world.

It's very hard to control a large mass at the end of a long stick. Lack of motion in the foot, by itself, has very little ability alter the velocity of the center of mass. More below.

A third option is that the person chooses not to produce the forces. The person chooses to walk slower and with less ankle push and shorter strides. You don't see Charcot first rays with normal sensation.

Or the alternate explanation: Our treatment allows 1st MPJ motion so that we can use ankle push with less pain.

The chicken or the egg again. Fun as always,

Eric

 

Howard:

I believe that a better explanation of late midstance pronation is that this movement of the foot results when the dorsiflexion stiffness of the medial forefoot is much less than the lateral forefoot in late midstance. Then, as the center of pressure (CoP) moves more distally onto the forefoot during late midstance, there is a greater increase in medial forefoot dorsiflexion than in the lateral forefoot so that increased medial arch flattening and increased subtalar joint pronation occurs.

Because the medial forefoot dorsiflexes excessively, the magnitude of tensile force within the medial band of the plantar fascia increases which, in turn, increases the hallux plantarflexion moment. As a result of this increased resistance to hallux dorsiflexion (i.e. increased hallux dorsiflexion stiffness), functional hallux limitus occurs due to this medial longitudinal arch flattening and subtalar joint pronation. In other words, I believe that the primary cause of the medial longitudinal arch flattening that is often associated with functional hallux limitus is due to increased medial longitudinal arch compliance, not due to some "force dissipation mechanism", as your theory proposes.

 

Hi Eric,

I’m glad we don’t agree, or we would have nothing to discuss.

I don’t recall Howard telling the patient to take a few practice walks with longer strides. That being said, what would prompt the body to take longer strides?

I must have misunderstood you. I thought “Winter did not say that there was no hard wiring. It was my observations related to his work”, meant there was no hard wiring. Sorry.
By the way, the loss of the Babinski response is a normal developmental milestone and failure to lose it is associated with neurologic diseases.

I stand corrected. Modica did not measure power. However, he did find that there was no measurable change in the EMG of the medial gastroc and soleus with the ESA which means that no firing of these muscles is required to initiate swing.

The 6% of body weight is 100% of what the body could handle in the ESA. Interestingly, at 4% the net metabolic rate decreased by 20.5%, so the idea that 1% of body weight is equal to 1% force is not accurate.

First of all Modica did not test the hip flexors, just the rectus femoris which is a knee extensor and hip flexor. More importantly, the ESA pulled the leg forward, not upwardly; and most importantly, the plantar flexor activity was unchanged.

I don’t think support equals pushoff. Do you?

Regards,

Stanley

 

Kevin,

Interesting reply....except for the following. You are supposing that the CoP is actually advancing in some predictable fashion during the step. However, this is not always the case....in fact, it commonly delays considerably, and this is what in-shoe pressure analysis demonstrates. It is these delays in CoP advancement with a concurrent advancement of the CoM which creates the "rock and a hard place" analogy. The CoP can advance efficiently when the foot moves through its normal sagittal plane range. If the foot fails to permit this motion, the CoP delays or slows, and the support system eventually collapses. It is not any single step, of course, but the millions and millions of steps that patients take prior to our seeing them that creates their mechanical predicament. My observations have shown me that you need a lot less orthotic to produce a positive outcome when the goal is to promote sagittal plane facilitation vs trying to control how much a foot pronates.

Howard

 

Kevin;

I don't disagree with you statements above and I applaud you for attempting to redefine what is happening adn why in the foot and forefoot.

Howard is correct in his statement though. What you describe above is not an ideal process of foot function, therefore it is a "force dissipation mechanism" as Howard described.

If the foot were to roll forward with ample AJ ROM and 1st mpj ROM in a timely fashion then there would be both energy storage from contact and then energy release from late midstance thru toe-off. All of which would be as efficient as possible to allow continuation of perpetual walking with as little energy usage as possible.

When the foot or ankle does not function ideally from stride to stride, then the forces that should be stored for release of energy must disipate somewhere. This will then lead to "tissue stress" with or without any real or perceived avoidance of pain.

Bruce

 

Hi Stanley,

Gait changes don't occur immediately. The body would take longer strides because it is more efficient method of walking. Now, that the 1st MPJ has more range of motion and it hurts less longer strides can be taken. Pain avoidance overrides efficiency.

I knew that it was a normal milestone. What I don't know is why the change occurs.

I guess we will have to agree to disagree on what the Modica data mean.

Why could the body not handle greater than 6% of body weight with the ESA? It caused soreness of the knee flexors. The knee flexors slow the swing leg down at the end of swing. The ESA also increased step frequency because of decreased swing time even though the subjects were running at the same velocity. The purpose of the ESA was to initiate swing. As force is added in the ESA, at some point you are going to equal what the body needs for swing. I am making an assumption from the above that at greater than 4% of body weight the body actually wants to slow the swing leg down. Yes, there is an increase in aerobic efficiency up to 4%, but that doesn't mean that efficiency will not start to decrease because of increased knee flexor use as more force is added to the ESA. So, I think that it is a good assumption that 4% of body weight, applied at the foot, is what is required to make swing happen.

The ESA is designed to reduce the need for hip flexors and the one hip flexor measured showed a dramatic decrease in EMG activity. How else do you explain the 20% increase in aerobic efficiency other than decreased hip flexor activity? Especially since there was no change in gatroc soleus EMG activity and variable change in biceps femoris activity.

The fact that the ESA is only pulling forward helps my explanation of why the gastroc soleus EMG does not change. The swing leg has to be lifted to prevent tripping. (There must be a vertical force from somewhere.) The choices of joints that can do this are hip flexion, knee flexion and ankle planar flexion. There is a decrease in activity in the only hip flexor measured. Knee flexion might be part of it, but it sends the foot in the wrong direction for swing. Ankle plantar flexion is the most likely candidate for lifting the trailing leg. So, instead of providing forward propulsion it provides lift of the leg. That would explain why there was no change in the EMG. If they had measured ankle joint motion they may have seen this.

It's the same muscle moment. Support, as described above, requires an ankle plantar flexion moment and push off requires an ankle plantar flexion moment. Yes there is a definitional difference. But, these moments are produced by the same muscle at the same instant in time. Moments are additive. A small increase in muscle force could produce support and propulsion. Possibly so small that you may not be able to see it on EMG. (Propulsion, in this sense, is a posterior to anterior force applied by the ground to the foot.)

Regards,

Eric Fuller

 

Kevin, Howard,

To reiterate the discussions that we've had on this before. There is more than one way to explain the delay in calcaneal unweighting. They are not mutually exclusive. One explanation is that since the foot is more flexible (decreased dorsiflexion stiffness) it is more difficult to load the forefoot. This occurs because the foot is flexing, and the forefooot is not accepting weight.

Another explanation is pain avoidance. When there is tension in the Achilles tendon there is an anterior shift in the center of pressure and an increased bending moment. A person, who wanted to avoid midfoot stress, could choose to walk with less gastroc and soleus activity and this would show a delay in calcaneal unweigting. An orthosis that successfully reduced midofoot stress/ or pain, would allow the person to use their gastroc and soleus more and you would see a more "normal" progression of the center of pressure.

I agree that you don't have to have aggressive posting to reduce pain in the foot and produce a more normal center of pressure path. Again, we agree on the observations, we are just disagreeing on the explanations.

Regards, Eric Fuller

 

Eric,

Its great you are keeping it simple!!! That said, there is always more than one way to look at anything...and it is the multiple views that provide the ultimate in understanding. Thanks for your insight.

Now, I see many, many patients who are referred to me for management of their chronic lower back pain. (My published resolution rates in medical endpoint LBP subjects is > 84%.) They most often do not have any foot symptoms, nor have they ever. Yet, they exhibit a very pronounced sagittal plane restriction at the foot level, and compensate through the entire kinetic chain for this. Since pain avoidance (which I absolutely agree can exist) is not the issue in these cases, and there not necessarily any evidence of decreased forefoot dorsiflexion stiffness (ie, flexible flat feet), then it would seem that a pure sagittal plane restriction can be a very viable entity. I do fully appreciate that other explanations can exist, and I do see these from time to time, but the vast majority of the patients I see are negatively impacted by their sagittal plane facilitation issues.

Considering your agreement that orthotics that do not have to address frontal plane issues (ie, non-agressive RF posting...see above) to be effective, how does this jive with all you have written about the necessity of reducing the pronatory force moments using aggressive RF posts?

Howard

 

My answer to the "my feet don't hurt, my back does" point has always been: See how effective walking without propulsion is in preventing foot pain.

Regarding medial skives and rearfoot posting. A lot of feet that exhibit late stance phase pronation are in fact oversupinators (those with more laterally positioned STJ axes). What happens, in these feet, as the Achilles begins to lift the heel it also causes a supination moment and the peroneals have to kick in to prevent excessive supination. In these feet an orthotic shell acts a guide to prevent "excessive" pronation. Again the pain avoidance theory is working here as pronating into the orthotic shell will cause pain. An orthosis with a rearfoot varus wedge effect will not work for these people.

On the other hand those with more medially deviated STJ axes do quite well with Medial heel skives.

Regards,

Eric Fuller

 

Eric;
So you suggest to your patients to limp so that they can avoid foot pain? But you would encourage someone w/o foot pain, and with back pain to try to actively propulse even though you are convinced they are walking that way because they have foot pain? :dizzy:I'd love to see the outcomes on that study. :bash:

Finally, your idea that a patient with a laterally deviated STJ will fire the peroneals and over pronate is nonsense.

These patients have a lateral deviated STJ along with AJE and decreased DFion stiffness. The achilles and AJE work hand in hand to shut down the effectiveness of teh PL and thereby the 1st ray hypermobility will follow.

They will be unable to effectively fire the Peroneus longus if indeed a pronatory problem is in effect here in relation to a FnHL. They may continue to fire their P. Brevis or Tertius to try to pronate the foot thereby causing some lateral foot pain.

To effectively treat these patients you need to address the AJE with manipulation, heel lifts, adn by addressing the LLD that is usually present. Then a lateral FF valgus post is necessary for these patients, along with a medial heel skive to properly guide them into late midstance supination and allow all the peroneals to fire adequately.

The medial heel skive is necessary for a proprioceptive feedback response so the body will be fooled into thinking it has made proper contact adn will no longer need to supinate as much. It will also increase the medial pressures and help to bring the CoF medial so long as the post is not too high, which can then push the CoF more lateral than before. Some of these patients must be posted in valgus from the heel to the FF as well to get a realistic response.

I can see why you state that you "believe" in the tissue stress model so much Eric. You don't have a shred of evidence to show that there is really a pain response, but you "believe" there is. igs:

Bruce

 

Bruce,

I'm sorry for what you felt was a personal attack earlier. At the time I was tired of hearing that the ankle cannot push the leg into swing. After seeing this thread I can now see how there are some articles that support the notion that ankle does not push the leg into swing. I still the best measure of whether or not the ankle can push the leg into swing is measurements using ankle power. We can agree to disagree on this.

Bruce, if you are going to call my ideas nonsense you could at least explain your reasoning. Above you describe how you would treat a patient, but you do not address why my idea is nonsense.

You should see the video that Kevin made when he was the biomechanics fellow at CCPM of a rigid forefoot valgus gait. It is a remarkable example of a foot that exhibits late stance phase pronation in an over supinated foot. It was also a very rigid foot, so I don't think you can come up with a better explanation of why this foot pronated in late stance phase other than peroneal activity.

Regarding pain avoidance theory and lack of evidence for it. Explain to me why people limp when they hurt if it is not to avoid pain. Explain why charcot joints happen in the presence of neuropathy and they don't happen with normal sensation.

Regards,
Eric Fuller

 

Bruce:

Actually, this isn't Eric's idea, it is John Weed's idea that the peroneals cause late midstance pronation in patients with this foot type. I agree with Dr. Fuller and Dr. Weed. I can think of other examples of "nonsense" within certain podiatric biomechanical theories, but don't think we should use the term "nonsense" if we are to keep this discussion civil and friendly. If you want say you disagree, that certainly seems sufficient for us to understand your meaning.

 

Eric;

A rigid supinated foot that is capable of pronation in late midstance is not a foot that overpronates in late midstance. There is a huge discrepancy in your statements. That is why I said nonsense.

I did explain my reasoning as well when I stated that AJE and a tight tendo-achilles complex will cause the Peroneus Longus to become inhibited. Reference "Biomechanics of the First Ray Part V: The effect of Equinus Deformity" C. Johnson, J. Christensen, JFAS Vol 44, #1, March / April '05.

Finally regarding your theory and examples above. I do not have to explain anything, you do. I have made my explanations plain over and over again just as you have done. When you stick to power and kinetic explanations then I listen and I learn and we can challenge each other. When you state a belief that something is true then there is no opportunity for debate.

Bruce

 

Howard:

I don't "suppose", as you stated above, that CoP velocity does not change. It will not progress as rapidly anteriorly if there is decreased forefoot dorsiflexion stiffness, and the forefoot dorsiflexes on the rearfoot excessively during late midstance, which, again, is the cause of functional hallux limitus. The stump we are going around is the same old chicken and egg story that we have been discussing for years. I'm growing tired of it for now as I'm sure you are. But it is good that the members of Podiatry Arena have been exposed to your views on the subject. Thanks for that.

 

Bruce:

I fully understand your and Howard's explanation for your observations. However, I do not agree with your explanations. There are other very reasonable explanations that to me, and others, make even better biomechanical sense. We will need to agree to disagree for now since I am growing tired of beating the same old horse over and over again.

Happy Holidays!:drinks

 

Hi Eric,

Eric, I am trying to understand this whole concept of pain avoidance. I guess you would say it is a conditioned response. So every time the little boy puts his hand in the flame it gets burned. After a while he learns (rather quickly) not to put his hand in the flame. Now if there were a flame that would burn at a lower temperature because of a different fuel, no matter how long the boy was in the room, he would not put his hand in the flame because he believes it will be painful (just like your pediatric patients believe that your injections are painful, no matter what you say). The body has associated long strides with the pain. It makes no sense to me that if there is pain avoidance; the body would go away from its conditioning just because it is more efficient. How does it know this more efficient gait would result in less pain? Why would it believe it? If as you say "Pain avoidance overrides efficiency" then why would in this case efficiency override pain avoidance?

It has to do with development of the nervous system.
http://pennhealth.com/ency/article/003294.htm

Modica said “In conclusion, we find that leg swing requires 20% of the net energy consumed in running. Neither MG, Sol, nor RF muscles contribute to leg swing initiation; however, RF does play a significant role in leg swing propagation.” It was a straight forward paper with straight forward results and straight forward conclusions. You can choose to disagree with him. You can also choose to disagree with Gottschall who studied walking,
(http://jap.physiology.org/cgi/content/full/99/1/23)
who writes “During the ESA conditions, neither the MG mEMG nor the Sol mEMG was significantly affected by the ESA forces. During the AHF conditions, we found that the MG mEMG decreased during AHF-only trials but that the Sol mEMG did not change (10). Similar to previous studies (24, 29), our temporal results for normal walking showed that, on average, neither the MG nor the Sol was active past 52% of the stride. It is possible that the force generated by these ankle extensors at the end of the first half of stance phase can produce forward acceleration of the limb. But, our results suggest that neither the MG nor Sol directly initiates or propagates leg swing.”

The reason for the soreness was there was no cable clamp applied to the ESA. In the Gottschall study, they added a cable clamp, and they found the optimum was 7%

The ESA is designed to assist in swing. Modica did not measure the iliopsoas, but Gottschall did. I agree that the hip flexors showed a dramatic decrease in activity with the ESA.

The muscle that lifts the foot so you don’t trip is the Anterior tibial. Gottschall found that when using the ESA, ”The TA mEMG was significantly higher during swing initiation, propagation, and termination”.

Eric, do you believe in homeopathy?

Regards,

Stanley

 

Eric,

In diabetes, the first findings are loss of the dorsal columns that transmit: two point touch, vibration, and proprioception.
If you remember, pain was the lateral spinal thalamic tracts. This happens later.
Charcot happens because of loss of proprioception. The fact that there is no pain sensation is an incidental finding.

Regards,

Stanley

 

Thanks for providing an explanation. It appears we just had a terminology problem. Do think that deserves to be called nonsense?

Could you explain how this statement has something to do with my statement about late stance phase pronation being caused by peroneal activity. (Yes, it was John Weed's idea.) Did you leave something out?

You said that I don't have a shred of evidence for the pain avoidance thoery. I was giving two commonly seen examples related to pain avoidance. Do you think the examples I gave are not supportive of pain avoidance altering gait?

Regards,

Eric Fuller

 

To take your analogy a little farther. The boy doesn't have to walk through the fire to get anywhere. If the boy had had a reason to constantly test the temperature he would find out about the lower temperature. In walking you are often required to make moves that would test your self imposed limitations. When you test the limitations you would learn that once painful, but efficient motions can be done pain free.

From the Gottshall article results section referring to mean EMG
As we have reported previously (10), during the AHF-only trials, the MG mEMG was lower during the propulsive phase of stance; however, the Sol mEMG did not change compared with the normal walking trials (Fig. 8). With 10% AHF only, the MG mEMG was 55% lower than the normal walking magnitude (P < 0.0001), but the Sol mEMG did not differ compared with normal walking (P = 0.16). Moreover, when ESA was combined with AHF, the mEMG of neither the MG nor the Sol differed from the AHF-only trial.

Perhaps, you can help me here. They seemed to have shown that the medial gastroc was 55% lower than normal walking the AHF and there was no difference between the AHF combined with the ESA. Wouldn't that imply that there was a 55% difference between normal walking and the combined AHF and ESA? How do they conclude that there was no difference with the medial gastroc?

Additionally the study noticed, but did not explain that there was decrease in propulsive force with the ESA. Yes, less propulsive force is needed with the ESA, but why did horizontal propulsive force from the ground decrease?

They note an increase in Tib Ant activity. This would produce a dorsiflexion moment that would decrease the net plantar flexion moment at the ankle. So, if there is co contraction the net moment would be reduced, but the soleus EMG would remain high. This could explain the decrease in ground reaction force. It's a shame they did not measure motion (or joint power).

Actually, the Gottschall pilot study tested 1, 3, 5, and 7% and found that 5% had the lowest energy consumption. There was an increase in energy consumption between 5 and 7% BW for the ESA. They also mentioned the probable cause of the increased energy expenditure was slowing of the swing leg.

From their data, I still think that a good assumption of force applied to the foot of about 4-5% of BW is required for swing. (The force at the hip would have to be higher because the hip muscles have a much shorter lever arm about the hip joint as compared to lever arm from ground reaction force at the hip.

The question that I have is lifting the foot enough. Doesn't the whole leg have to be lifted?

I'm skeptical, but have not studied it. For me to believe I would have to see physiological and chemical analysis to back up the claims.

Regards,

Eric

 

Does Charcot always happen with proprioception absent and pain intact? When the proprioception is gone is pain sensation still 100% intact? I think I can see how injury could occur with the absence of proprioception and pain intact, but is there more when pain is gone? Those folks are certainly more likely to keep walking on it with the absence of pain.

Regards,

Eric

 

Eric;
in the context of our discussion I found your example to be nonsensical. I apologize for seeming harsh or short.

I think you need to clarify further. I now realize you are talking about a rigidly supinated foot that will pronate at the STJ, but still have a laterally deviated axis. You then state that it will pronate in late stance. This is where you need to clarify further for me. This foot type will never truly pronate except positionally once the heel has left the ground. That is not the same as late stance phase pronation in my book, or in Root's I think.

Just because the peroneals appear to be visually firing at this stage and the foot positionally is pronating does not mean that is exactly what is going on. If I recall correctly, patients with a rigid cavus foot type are prone to achiles inhibition or weakness which then allows the flexors to become overactive. Considering the peroneals are flexors and also will be inhibited both by AJE and Achilles tightness, they may be overactive to subsitute for the inhibition or weakness of teh achilles at heel lift. The foot is already very stable and should roll right thru the 1st mpj so there is no real reason for the PL to become over active. But, if the 1st ray in this patient was hypermobile, then my comments from before do apply.

Finally, how does an insensate foot that has no pain response apply to your stress theory? They can't feel and have no reason to walk differently so how does that even make sense? I do not understand this example and what you are intending it to show at all. If anything Eric, it seems to ratify my ideas much more.

Bruce

 

Pronation is when the subtalar joint moves from a more supinated position to a more pronated position. Bruce, what do you mean by truly pronate? Midstance phase is the time between forefoot loading and heel off. Late midstance stance phase would be in the latter half of the that time. I think Root et al. would agree with that definition. What is stance phase pronation in your book?

Do you have a site or an explation of why achilles inhibition would occur in a rigid cavus foot?

The peroneals are not flexors of the ankle joint (you are referring to the ankle joint?) Hicks described them as very minimal plantar flexors. I've done work with cadavers where I've looked at tendon motion with joint movement. The peroneals barely move with ankle joint motoin and move quite a bit a movement with STJ motion.

Why do you think that flexors will be inhibited by AJE ?(AJE = ankle joint equinous?) and Achilles tightness?

I'll try again. The pain avoidance principle: When people hurt the change their gait to avoid pain. They change their gait to reduce stress on the injured structure. Limping reduces stress on the injured foot.

Injury is caused by high stress on anatomical structures. Injury also causes pain. Those without normal sensation will not walk with a pain avoidance gait and continually impart high stresses to an injured structure. Continued high stress will lead to Charcot joints.

Using the tissue stress approach you can look at basic foot mechanics. For example functional hallux limtus is caused by the unwinding of the windlass mechanism. Things that cause the windlass to unwind (STJ pronation, arch flattening) will tend to increase tension in structures attached to the plantar aspect of the base of the proximal phalanx. This increased tension will cause an increased plantar flexion moment on the hallux and will result in functional hallux limitus.

Or with the tissue stress approach you can look at other factors of stress like relative muscle activity. For example arch flattening is increased with increased tension in the Achilles tendon. So, if someone was feeling stress in their foot from high tension in the plantar fascia, an individual could choose to walk with less tension in the Achilles tendon. (Just as someone chooses to limp when their foot hurts.) So, when you use the tissue stress approach you should also look at input forces from the muscles and admit that they are not the same every step, day in and day out.

So in the tissue stress approach to treatment of functional hallux limitus you figure out what decreases tension in the plantar fascia and you design your orthosis to reduce tension in the platar fascia.

So, Bruce, in your book, what causes functional hallux limitus and what does an orthosis do to cure it?

On pain avoidance and asymptomatic feet. How often, with functional hallux limitus patients, do you see asymptomatic hperextension of the 1st IPJ? Even though the hyperextension is now asymptomatic, do you think it was painful at some time? Would it become painful if someone increased stress on the IPJ?

Regards,

Eric

 

Hi Eric,

I enjoy your insight, and how it makes me look at everything a lot more closely.

In walking, you don’t have to take longer strides to get anywhere. If someone is testing their self imposed limitations, then this is not avoidance. The definition of avoidance is:
avoidance - deliberately avoiding; keeping away from or preventing from happening
http://www.thefreedictionary.com/avoidance

You originally said the body avoids pain. This brings up a larger question. If the body is avoiding pain, then wouldn’t patients always come in with a chief complaint of a gait disturbance (limp)? My patients come in because of pain. If there is a hallux limitis, and they take shorter strides, then there would be no deforming forces from the hallux limitus. So why are they coming in with plantar fasciitis. There are a lot of conditions that don’t always hurt, and they come in with a secondary problem. For instance if a patient is a runner, and they do some speed work in the spring, they may feel a little tweak in the back. It will be asymptomatic, but a week later they will develop Iliotibial band syndrome on that side due to the functional shortage of the posterior innominate. The sacroiliac joint is dysfunctional and asymptomatic, but the knee is symptomatic. If the patient received a cortisone injection in the knee, the pain would be gone, but they would get recurrence.
This part of our discussion has followed a very circuitous route. I would offer a compromise, that would satisfy me, and should satisfy you (I hope). This is what I propose: There are mechanoreceptors in the joints, tendons and muscles that are responsible for triggering and modifying reflexes required for gait. The stimulation of the mechanoreceptors modify gait and prevent normal gait. This would explain why we do not see pain all the time, and it would explain why there is pain (the mechanoreceptors do not make a gait change). It would also explain why gait changes back and why sometimes it doesn’t (the mechanoreceptors are malfunctioning)

The writing is confusing (don’t try reading it at 3AM and expect to get it all). They mean that in the AHF only trial there was a decrease in the MG and not the Sol (compared to no EHF or ESA). In the AHF +ESA there was a similar decrease (compared to no EHF or ESA).

"Thus the ESA alone inadvertently aided forward propulsion", (p26 beginning of the results section)

The Tib Ant and Soleus are not active at the same time. (see fig. 6 page 27 on the bottom of the page)

You’re right, I misinterpreted the statement "With 7% ESA, the net metabolic rate of walking decreased to 89% of the normal walking metabolic rate, which was greater than with 5% ESA" See Eric, I said the writing is a little confusing.

Yes and they show the Iliopsoas being active at the beginning of swing with the rectus femoris (in the running article (Modica), the rectus femoris was active later in swing)

The reason I asked is that you are talking about things “Possibly so small that you may not be able to see it on EMG". It is my understanding that you will see EMG activity before you will see motion.

Eric, the key statement in the study is: “Similar to previous studies (24, 29), our temporal results for normal walking showed that, on average, neither the MG nor the Sol was active past 52% of the stride. It is possible that the force generated by these ankle extensors at the end of the first half of stance phase can produce forward acceleration of the limb. But, our results suggest that neither the MG nor Sol directly initiates or propagates leg swing.”

Again, I want to reiterate that the only thing that makes sense when combining this study and the Winter study (which I am still waiting for) is storage of energy in the soft tissues will power the ankle at propulsion.

Regards,

Stanley

 

Eric;

enough! I am not being very nice right now, and that is not conducive to a rational debate. I apologize for that.

You and Stanley will have to carry on without me until I am in a better state of mind.

My apologies and I sincerely hope you will have a happy holiday season.

apologetically;

Bruce

 

Bruce:

Come on back when things have calmed down for you since I, and I'm sure many of us, enjoy your valuable contributions to these discussions. Hope you and your family have a Great Christmas!

 

Stanley, Look at figure 8 in the paper. It clearly shows the medial gastroc is firing less with all of the externally added force conditions. As the medial gastroc is an ankle plantar flexor and Neptune has shown the gastroc is more likely to initiate swing than the soleus, the data clearly support the notion that the medial gastorc is adding to swing in stark contrast to their conclusions.

Additionally, the decrease in anterior postior shear force correlates with the decrease in gastroc activity. Anterior to posterior shear would be caused by ankle push that becomes less when there is less activity in the medial gastroc.

Regards,

Eric Fuller