Query
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When the foot is cast / scanned it is done in the with foot ?perpendicular? to the lower leg, with the MTJ maximally dorsiflexed, yes?
After the foot orthoses is made from that ?foot morphology? it is used in footwear which mostly have a heel differential (if that?s the correct term) so surely the foot doesn't function in the cast / scanned morphology.
An orthotic heel grind addresses the differential but doesn't address the required change for the upper surface of the foot orthoses?
The heel would act as a wedge with distal end thickest applying an additional rearfoot dorsiflexory moment?
thanks, mark
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1) Orthoses transmit loads from the body through their structure to the shoe and so to the ground, To produce static equilibrium, an orthosis must provide an equal and opposite reaction (Newton's 3rd Law of Motion)
2) When loads are applied to an orthosis, the orthosis tries to absorb its effects by developing internal forces that vary from one point to another. The intensity of these internal forces is the stress
3) When subjected to external loads, orthoses change their shape; though sometimes imperceptibly. This change in shape is termed displacement or deformation and is measured by the mechanical strain
4) The necessary orthosis reaction force is generated by the stress caused by the action of the loads within the orthosis material, and by the ensuing strain in the elements of the orthosis structure
An orthosis "works" therapeutically either psychologically (placebo) or via its mechanical effects. These mechanical effects may either have a direct mechanical influence on the locomotor apparatus or a neuromotor effect (or both), either way these two effects are reliant upon the three characteristics of foot orthoses which may influence reaction forces at the foot/orthosis interface:
1) the surface topography at the foot/orthosis interface
2) the load/ deformation characteristics at the foot/ orthosis interface
3) the frictional characteristics at the foot/ orthosis interface
Foot orthoses do not work by holding the foot in the position it was cast in. An orthosis works by altering the magnitude and temporal patterns of reaction forces at the foot/orthosis interface. The magnitude and temporal patterns of the reaction forces at the foot's interface alter every time we take a step whether onto the same same surface or a different one. They will also alter when we place a foot orthosis in a different shoe, regardless of whether the foot orthosis is a so called "shank dependent" or "shank independent device"; always hated those terms, not least because the reaction forces generated at the foot/orthosis interface of a so called "shank-independent device" are in no way independent of the shank, nor the rest of the shoe. The shoe + orthosis combination always influences reaction forces at the foot/orthosis interface whether the device is "shank independent" or not. Might not be the same influence, in the same shoes, but the reaction forces at the foot/orthoses interface are influenced by the "shank" and moreover the rest of the shoe in which they are worn as much as the type of orthosis placed within the given shoe, always- end of story.
Take two shoes with different shank characteristics, place the same, so called "shank-independent devices" in the different shoes. Will the reaction forces be identical in the two different shoes? No. Viz the reaction forces generated at the foot/orthosis interface are not "independent" of the shank within the shoe in which they are being worn. Thus, the term "shank-independent orthoses" has no place in modern podiatry since it is a misnomer. ;-)
There is more but it's dinner time. I'll leave you with this thought though: step to step variability in reaction forces are real; the variation in the surface angulation of the environmental topography that we function upon is often greater than the degree of posting placed into the orthosis; shoe to shoe+ orthoses variation is real, yet still the same pair of foot orthoses seem to "work" therapeutically in the wide variety of environments and locomotor tasks that we subject them to on a daily basis. How does that work? https://www.youtube.com/watch?v=MEt_piATFVk -
The "cast" is a way of communicating with the lab that makes the orthoitic. The cast will give you the length of the foot and the medial and lateral arch heights and a couple of other things. The cast does not give the relationship of the foot to the leg when the cast was taken. The lab may or may not incorporate the shape into the finished product. (Arch fill) Your prescription may instruct the lab to alter the shape of the orthotic relative to the shape of the cast (Intrinsic forefoot post, medial heel skive)
There has been a concept prevalent in the podiatric community that casting the foot in a certain position will make the foot function in, or closer to, the position that the foot was casted in when the foot stands on the orthotic made from that cast. I call this concept voodoo biomechanics.
The orthotic shell can apply forces to the foot in a different location than the ground does. How those forces differ is dependent on the shape of the orthotic. The forces applied to the foot may make the person choose to alter the relative activation of the muscles of the foot. The change in location of ground reactive force, or the change in muscle activation will hopefully reduce the stress on the anatomical structure you have designed your orthotic to protect. -
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Goodaye Simon,
Not sure I expressed myself well.
Thanks for the post, brilliant, essential reading for all podiatrists, however, since following your posts and reading many of your journal articles/opinions I am aware (except for the inappropriate use of the shank-independent term) and comprehend all the post's material, and certainly don't query any of it.
Also wouldn't the same applies for shank-dependent foot orthoses.
thanks, amazing resource PA and its members contribute, mark -
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and surely, which is my query, the shape of the shank.
thanks Eric -
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Also 3) re. friction characteristics of the orthoses topcover
Wouldn't you always use the material with the most friction?
mark -
In terms of friction, really I have been lazy in referriing to the foot-orthosis interface. Actually we have the orthosis/hosiery interface and the hosiery/foot interface. Obviously we want some degree of coupling between the orthosis/hosiery interface, but we also might require that some of the shearing occurs here, rather than at the hosiery/foot interface. If we have too much friction at the orthosis/hosiery interface then the shearing may occur at the hosiery/foot interface or within the subcutaneous tissues of the plantar foot- this may not be desirable in diabetic neuropathic patients. Jo Paton wrote about this in one of her papers or maybe it was her PhD thesis. -
Thanks again Simon, excellent, now i'm with you
as for friction / shear, comprehend, great reply, and will certainly search for Jo Paton's work
te deseo lo major, mark -
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http://www.sciencedirect.com/science/article/pii/S0968016006000135
Many of the articles you're probably referring to, were written by orthopedists, with several Podiatrists "buying into" their studies. I'm not one of them. Time to go back to the basics. -
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I guess the orthos in my region haven't read the tissue stress theory about why lateral wedges work. Through their own trial and error, they have decided, collectively, to disregard the earlier studies...again...because they don't really work. One of the problems I see is many of the researchers are still of the belief that causation lies in the frontal plane. -
I enjoyed reading the replies from Drs. Spooner and Fuller regarding your questions. Let me try to add a few more tidbits of information.
Regardless of how the subtalar joint (STJ) is positioned during negative casting/scanning (e.g. supinated from neutral, neutral, pronated from neutral,or even maximally pronated), the resultant orthosis made from that negative cast/scan will not necessarily "hold" the STJ in the same rotational position that the STJ was cast/scanned in. For example, you could actually cast/scan a foot in the maximally supinated STJ rotational position for orthoses and have that patient function with their STJ in the maximally pronated position if, 1) the foot had sufficient internal and/or external STJ pronation moments acting on it or, 2) if the orthosis generated insufficient external STJ supination moments by mechanical contact with the plantar foot to overcome the excessive magnitudes of STJ pronation moments.
I remember discussing with Dr. John Weed something along these lines in one of my many private discussion with him during my second and third years of podiatry school. I told him during my second year of podiatry school that it made no sense to balance the heel of the positive cast in a vertical position if the patient's neutral calcaneal stance position was 6 degrees inverted and if the goal of the orthosis was to have the foot function in the STJ neutral position. He smiled that I asked him that question since I think he wasn't used to having students question him like that. He indicated that indeed this was a big problem in trying to understand how foot orthoses worked.
Foot orthoses don't "hold the STJ in neutral position", don't "lock the midtarsal joint" and they don't "prevent compensation for rearfoot and forefoot deformities" as we were taught over and over again during the 1970s and 1980s by the STJ Neutral Theorists.
Rather, foot orthoses function by altering the magnitude, plantar locations and temporal patterns of ground reaction force (GRF) acting on the plantar foot during weightbearing activities. This is why, then that in a foot with a severely medially deviated STJ axis , it is possibly to cast that foot in the maximally supinated STJ position for an orthosis and still have that foot function on that "maximally supinated orthosis" in a maximally pronated STJ position. This inability of a "maximally supinated orthosis" to be unable to supinate a foot out of the maximally pronated STJ position can occur because the orthosis did not have the mechanical ability to sufficiently alter the magnitudes, plantar locations and temporal patterns of GRF to generate enough external STJ supination moments to overcome the STJ pronation moment caused by the severely medially deviated STJ axis foot interacting mechanically with the ground.
One other comment I wanted to make was in regard to your question on the effects of heel height differential (HHD) on foot orthosis function. [Heel height differential is defined as difference in thickness of the shoe sole plantar to the central heel and the thickness of the shoe sole plantar to metatarsal heads.] This, Mark, is an extremely important concept clinically and one that has had very little research done on it. I have discussed this important factor over the past quarter century in my Precision Intricast Newsletter Books.
For example, it is quite common clinically to have a patient tell me that the medial longitudinal arch (MLA) of their foot orthosis is quite uncomfortable or intolerable in a shoe with a low HHD only to then put a heel lift under the rearfoot post of the orthosis or put the same orthosis into a shoe with a higher HHD and then have the orthosis become much more comfortable for the patient.
Did the shape of the orthosis change when it was placed from a low HHD shoe to a higher HHD shoe? No. What then did change? What did change was the sagittal plane angulation of the orthosis to the ground and also the dynamic function of the foot on top of the orthosis. The orthosis shape stayed the same but the foot now is mechanically interacting with the orthosis differently due to the change in magnitudes, plantar locations and temporal patterns of GRF due to the difference in shoe sole geometry.
In other words, Mark, both shoes of different sole geometries and foot orthoses of different constructions produce their mechanical actions on the foot and lower extremity by altering the magnitudes, plantar locations and temporal patterns of GRF acting on the foot during weightbearing activities. Therefore, one cannot exclude shoes from the combined shoe-orthosis mechanical effect any more than one can exclude orthoses from the combined shoe-orthosis mechanical effect that occur on the foot and lower extremity during weightbearing activities.
Both the shoe and the foot orthosis function in similar mechanical manners, by changing GRF on the plantar foot. The intelligent clinician who fully understands these concepts will then realize that 1) to achieve optimal foot orthosis function, the shoe geometry may need to be altered and, 2) to achieve optimal foot orthosis function, the foot orthosis geometry may need to be altered for every shoe that has a significantly different construction, including such factors as HHD differences. Practically, this means that multiple pairs of custom foot orthosis may be required for patients who wear shoes of significantly different constructions in order to optimize the function of the orthosis inside the shoe.
Hope this helps. Good discussion.:drinks -
So many years later I fluked onto Podiatry-Arena and thank goodness for me (maybe not others)
Thanks Kevin, excellent as always, again compulsory reading for all podiatrists, mark -
Could you explain your "written by orthopedists" statement? Why do you trust the opinion of the orthopedists you know over the ones that wrote those papers?
Eric -
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This is also the problem with Root biomechanics. There is more bio than mechanics. Or more precisely there is a focus on motion while ignoring forces. You can understand so much more if you look at motion and forces. If you living only in the Root biomechanics world you are missing out on some understanding. You can't get any more basic than anatomy and physics.
Eric -
Quote from Eric Fuller in previous post,
" If you living only in the Root biomechanics world you are missing out on some understanding. You can't get any more basic than anatomy and physics."
Here in Australia there are so many guilty of same, despite Craig Payne and crew's attempts on PA and 'Boot Camps' to remedy this.
Realise this post is taking up space but couldn't resist highlighting the simple truth -
One of the problems I see in creating new descriptions is that, typical of doctors from various disciplines, we tend to make our science much harder than it really is. This thread is a perfect example. We have Dr. Fuller discussing anatomy and physics when describing why lateral extensions work in treating medial knee osteoarthritis, obviously forgetting that the ankle joint is a ginglymus, therefore still believing that the cause of DJD in the knee lies in the frontal, (coronal), plane. Then, we have Dr. Kirby relating a story about a conversation he had with Dr. Weed 30 years ago which, I guess, is supposed to persuade all of us that their theory had holes in it, therefore, was wrong. Newsflash: Theirs was a work in progress...but the very basics outlined in their book is correct. The fact that after 30 years, we haven't "filled in the blanks", (or holes), is more a testimony to our own failures...not theirs, IMO.
I asked this question on another couple of threads...multiple times, and did not get an answer. So I'll ask you the same: Can you name me one pathology that Tissue Stress Theory has resolved in Podiatry, that can't be/wasn't explained by Root Biomechanics? -
Well good on you, and since this post is meant for others, adieu
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Eric -
2) I haven't read the Tissue Stress Theory of HAV formation...but if it were given in...say...the last 5 years...you're comparing a theory that was formulated 5 years ago to one that is >30 years old? How generous of you. Just because you don't like a work in progress, and/or the explanation of a certain pathology, does not mean you need to throw the baby out with the bath water. Just tweek it...that's what I did when I resolved an medical dilemma that was 193 years old...and what "they" taught me in Biomechanics at CCPM didn't work right. Please provide me a link to the TST's explanation of formation of HAV...and let me discuss that. -
I proposed the HAV in my windlass paper that was in JAPMA in 1999. It is essentially the same as what McGlamry called reverse buckling with a few more diagrams with arrows.
Eric -
https://www.youtube.com/watch?v=7BSetRI_UH4&feature=youtu.be
2) There are many reasons why people develop bunions, actually. The shape of the first met head, presence of hypermobility, (eg., EDS), etc., notwithstanding. The windlass mechanism lies mainly in the sagittal plane, so I would think this "deforming" force would be down the list as contributing factors in my book. The FHL tendon also "pulls" in the sagittal plane...unless there's a deforming force which creates otherwise. Again, refer to the video, for in it lies some of the answers to the question of what causes bunions...those forces which lie mainly in the transverse and secondarily in the frontal planes.
Comparing an article that was published fairly recently, to a body of knowledge that was presented over 30 years ago is not quite fair. They say that medical knowledge doubles every 5 years...now, with the IT, I would say that time frame is greatly reduced. I remember Dr. Scherer giving a lecture on Biomechanics back in the early '80's when he took an 8X11" paper representing what we know about Biomechanics presently, and placing it on a rather large table which represented the total knowledge we need to know. In other words, he admitted that our knowledge was lacking...which pretty much echoes what I've tried to tell others here. -
Eric -
2) The forces you described are, IMO, minimal compared to GRF's and the patients weight, (basically one in the same). I never stated that round met heads CAUSE HAV...merely that they were contributory in expediting the development of that deformity. The development of bunions has more to do with the position, (and motion), of the first met as one enters the propulsive phase of gait, than with the proximal phalanx, (which is not even the insertion site of the FHL tendon). But I digress.
3) Like I wrote...medical knowledge doubled every 5 years prior to the IT...which has been reduced since that time. Root et al did not have all the answers...and perhaps their explanation was lacking...but their foray into defining what was normal is a step in the right direction. It gave us something to work with...to expand, test, discard...whatever...it was an outline given to us to complete...which we really haven't. I've read several articles about TST...heard lectures on the subject, read chapters in books on it, including yours in Lower Extremity Biomechanics Vol. I. Besides being a treatment for insomnia...I never really learned anything useful...something I could use to improve my patient's pathologies/complaints...seriously. When the authors fail at simplifying their material, they lose many in their audience. When that same material never really solves any pathology, it becomes even more problematic. Your chapter had lots of cool diagrams and illustrations...no doubt. Kevin's diagram 6.18 even showed the STJ position which he wrote about in 1989. One problem...that is not what I've determined in my own practice, with multitudes of patients. Kevin was very close to uncovering the cause of GP's in children...and I believe, RLS in adults. For some reason, he missed it. I showed a pic on another thread here at PA, of a patient with the bullet-hole sign, and I can easily prove there's no further pronation available with that foot at static stance. Yet most here have concluded that this foot is supinated...not maximally pronated. I'll get a video and post it for you to see. Am I discarding what was taught to me? Yes I am..at least on that topic....as well as applying varus wedge extensions to my orthotics...which are complete to the end of the toes as shown in my article. I have even redefined, for my patients' sake, forefoot varus. More on that later.
One of the problems, as I see it, is the dogmatic manner in which many Podiatrists lecture/attack the rest of us "commoners" about Biomechanics. It is on full display here at PA....aided and abetted by the powers that be. No wonder Dr. Phillips has abandoned posting on this site. Perhaps you should take pause and reflect on that. Hope it helps. -
Newton's third law: for every action there is an equal and opposite reaction. In my windlass paper, right after I described the forces on the proximal phalanx, I examined the forces from the proximal phalanx on the first metatarsal head (the equal and opposite reaction) When the distal to proximal force from the proximal phalanx, acting on the first metatarsal head, is not directly aligned with the proximal to distal force from the first cuneiform acting on the base of the metatarsal, in the transverse plane, then the metatarsal will adduct or abduct.
Root et al, did discuss bowstringing of the long tendons of the 1st mpj, but Don Green wrote and article in 1981 showing that bowstringing does not occur. The long tendons will also pull the distal and proximal phalanx back toward the first met. So, they do also contribute to the reverse buckling that occurs at the mpj.
Matt, do you want to try and explain how the position of the first met during propulsion causes bunions. An explanation will be better if it includes forces rather than just positions and motions.
Eric -
Jeff -
Maybe it was just me trying to find the errors. However, I don't recall much physics beyond chapter 2. Jeff, I can't find my copy of volume 2 right now. Are there any examples of application of physics that you think are worth bringing out as examples.
Eric -
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"The peroneus longus tendon has a relatively insignificant lever arm to produce ankle joint plantarfelxion or to decelerate forward momentum of the leg. It has a short lever arm to the subtalar joint axis and exerts a moderate pronation force at the subtalar joint. At the time the peroneus longus contracts, the leg is externally rotating and the foot is supinating at the subtalar joint. Contraction of the peroneus longus muscle exerts a slight decelerating effect upon this motion.
When the cuboid is stabilized by the soleus, during the midstance period, the cuboid becomes a pulley which controls the effectiveness of the peroneus longus tendon to stabilize the 1st ray and to plantarflex the medial side of the forefoot against the ground. In the late midstance and propulsive periods, the foot is in a supinated position at the subtalar joint. The insertion of the peroneus longus tendon at the base of the 1st ray is much higher from the ground than its pulley (cuboid). Contraction of the peroneus longus at this time imparts a strong plantarflexion force to the baase fo the 1st ray. The tendon also has a significant lever arm for pronating the forefoot about the longitudinal axis of the midtarsal joint so that the peroneus longus also tends to stabilize the entire medial plantar aspect of the forefoot against the ground during late midstance and early propulsion'.
As you can see from the above description by the authors, pulleys, lever arms, momentum, deceleration, rotation, force, etc. are all terms that are commonly used in and derive meaning from physics. I just picked this one section, of which there are many similar examples in the book, to illustrate how the elements of physics were used by the authors in an effort to provide a clearer understanding of foot function and pathology. So Root recognized that biomechanics, which has a foundation in physics, was critical to the future of his profession. And since many podiatrists didn't necessarily have a strong background in physics, he attempted to explain things in a practical manner. The chapter that was written primarily by Milt Willie, was an effort to provide a practical explanation of physics that would enable those without an adequate background in physics, a basis for understanding the application of physics that occurs in the rest of the book.
Jeff -
I think that "Normal and Abnormal" was the most complete book on foot and lower extremity biomechanics ever written in it's era (Root ML, Orien WP, Weed JH: Normal and Abnormal Function of the Foot. Clinical Biomechanics Corp., Los Angeles, CA, 1977.) While the book is now outdated, has some inaccuracies and does not contain many of the standard terms now used by the international biomechanics community, it still is a very readable book for the clinician that covers the basics of foot and lower extremity biomechanics.
I read the Normal and Abnormal cover to cover during my first year surgical residency (in 1983-1984) and again used it as a reference many times during my Biomechanics Fellowship (1984-1985). There was nothing like it as a reference during my student and residency/fellowship years. For these reasons, I am extremely grateful that Mert Root, John Weed and Bill Orien took the time to produce this book for the podiatric profession.
It is best, I believe, to think of "Normal and Abnormal" as one of the important references in the history of podiatric biomechanics that allowed others that followed Root, Weed and Orien to improve on their theories and mechanical explanations of pathological conditions of the foot and lower extremity. I would have a very hard time criticizing "Normal and Abnormal" since I know very, very well how much time and energy is required to publish a book. I think Root, Weed and Orien did a very admirable job in producing the books that they did for the era they lived in where foot biomechanics research was sparse and advanced biomechanics research equipment was primitive.
Just try to name any other book on foot and lower extremity biomechanics published between 1975 - 1995 that was more complete than "Normal and Abnormal"....I can't think of a single one. -
Aloha Mark,
It depends on how you make your orthotics.
If they are deforming plastic inserts on wedges of collapsing foam then probably not.
If they are contoured cradles on mechanical simple machine advanced composite spring levers then perhaps yes.
It depends on how you make your orthotics and what you want from them.
A hui hou,
Steve
Let's do a little new research into the concept.
https://bmedesign.engr.wisc.edu/projects/s16/enhanced_orthotics/ -
One idea come from Dananberg ( http://www.google.com/patents/US5782015 ). Other thoughts ?
Daniel -
In terms of orthotic shape, I guess we could say that all orthoses are shank dependent since they all rely on contact with the shoe. However, the more rigid the orthotic shell, the less dependent it is on the shank to maintain its shape. A Root type functional orthosis makes contact with the shoe at the lowest point of the heel seat (if un-posted) or on the entire plantar surface of the extrinsic rearfoot post (if posted) and along the anterior edge of the device. Some devices will contact the shoe along in lateral midfoot region along the 5th or 4th and 5th mets. Therefore the contour of the orthotic/foot interface is determined primarily by the shape of the shell provided the shell is sufficiently stiff, which is a requirement of a Root type functional orthotic. Therefore, the shoe can cant the device in the sagittal plane (usually slightly plantarflexed due to increased height of heel of shoe) or potentially in the frontal plane although most shoes will keep a properly constructed device close to the position that it was corrected to in the frontal plane (note that I'm referring to the position of the device in the shoe and not the position of the foot in the shoe). So an important advantage of this type of device as compared to a "shank dependent" device is that we don't have to try to fill the void between the shell and the shoe in order to retain the desired shape of the device.
A shank dependent device may require some fitting in order to sculpt the plantar surface of the device to match the contour of the shoe to prevent the shoe from altering the shape of the device in a negative manner at the orthotic/foot interface. If the shank dependent device was manufactured off of a corrected cast of the foot, then the goal would be to have the device maintain its device/cast interface shape once the device is fit to the shoe and properly loaded. One disadvantage of shank dependent devices is that they are more prone to shape change when used in different shoes with different interior (shank) contours.
Jeff
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