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Functional Hallux Limitus - old school or too important to miss?

Discussion in 'Biomechanics, Sports and Foot orthoses' started by jpaton, Mar 11, 2014.

  1. jpaton

    jpaton Welcome New Poster

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    Dear all

    I am currently involved in a research project the details of which are summarised below

    Problems with gait and balance are common in people who have had a stroke and can have a devastating impact on their lives. Limited mobility and poor balance may be caused by multiple factors, among which include foot and ankle dysfunction. Yet, the impact of specific ankle and foot impairments following stroke has received little attention. The purpose of the proposed research is to study foot and ankle problems after stroke and examine the effects on mobility and balance in community dwelling stroke survivors. This three phased multi-centred and multi-disciplinary study will explore the perspectives of individuals with stroke (phase 1), establish appropriate clinical measures to examine foot and ankle impairments after stroke (phase 2) and determine whether these impairments predict mobility, balance and falls in people with a stroke (phase 3). The work will support the development of targeted and appropriate multidisciplinary rehabilitation care after stroke.

    The research team are split over the inclusion of the best clinical measure of hallux dorsiflexion.

    Some feel hallux dorsiflexion seated to end range of motion would be appropriate it has shown good reliability and feasibility with individuals who have sufferred stroke.

    Others believe that a standing measure of hallux dorsiflexion until resistance is felt as a predictive measure of functional hallux limitus would be more likely to predit mobility balance and falls in people with stroke.

    The argument on one side is 'there is little consensus on FHL within the podiatric literature and it is embedded in old(er) paradigms of foot function'.

    Others think that 'measuring total hallux ROM non wieght bearing is of limited value because you will only be capturing a proportion of the population who function with a restricted ROM (ie those with OA of the 1st MTP for example), you will be excluding those who demonstrate functional hallux limitus in gait. Thus even if there is a correlation between a limitation in 1st MTP ROM in gait and function you would miss it.

    Its a bit like only recording people with a bonny restriction in ankle joint dorsiflexion as having limited ankle joint ROM and missing all those with a tight gastroc'.

    We would value your views to inform our research design and settle the dabate.


  2. Re: FHL - old school or too important to miss

    Hi Jo, Hope you are well.

    Why not measure hallux/ ankle dorsiflexion stiffness. i.e. the load/ deformation characteristics? The problem with non-weightbearing and weightbearing measure of RoM to "resistance" is that we do not know how much force is needed to achieve "resistance" (whatever that means). Two subjects may exhibit the same RoM, but the force required to achieve this might be very different; two examiners might not be applying the same force during testing yet reporting different RoM's. If you actually quantify the force being applied this negates this problem. Another issue is postural sway in standing, movement of the CoM anteriorly will increase hallux dorsiflexion stiffness. So while weightbearing is probably preferrable, in a swaying elderly population you might be better with seated measures. I'm assuming you are not looking for a dynamic measure?

    Hope that helps.
  3. FTSE

    FTSE Member

    Re: FHL - old school or too important to miss


    Just in case you haven't come across it - a Halstead & Redmond paper found "no association between maximum dorsiflexion observed during a static weight-bearing examination and that occurring at the same joint during walking". J Orthop Sports Ther. 2006; 36(8):550-556.

    The change in weight-bearing resistance when the foot is tested on an orthosis is impressive, but if there's no relation between that and real walking, it just adds to the mystery (to me) of why orthoses often work so well.

  4. efuller

    efuller MVP

    Re: FHL - old school or too important to miss

    Functional hallux limitus is a dynamic finding. Using the windalss model, one would predict that in the presence of high pronation moments there will be an increase in stiffness of the first mpj because of increased tension in the plantar fascia. There is more than one source of high pronation moments. In the foot with the medially positioned STJ axis, there will tend to be a high pronation moment from the ground. In the foot with a laterally positioned STJ axis there will often be a "reactive" increased pronation moment from the muscles to prevent an ankle sprain. So, you can see people who have hyperextension of their IPJ and deep impressions in their sockliner under the hallux, who have a relatively easy to dorsiflex hallux in static stance. On the other hand, those who have a difficult to dorsiflex hallux in stance, will tend to have the deep impression in their sockliner and hallux IPJ hyperextension. So, even if you were able to standardize the static stance test (as Simon pointed out) you would still tend to miss some people with functional hallux limitus.

    The research question is interesting. It would be interesting to tease out if weakness in one specific muscle was more important than some other muscle in predicting falls. It would also be interesting to correlate STJ axis position in the transverse plane with falls. You would also think that sensory deficit would be important too.

    What measures are you considering?

  5. Re: FHL - old school or too important to miss

    Agreed, Eric.

    Of course the other factor of significance in hallux dorsiflexion during "real world" function is the footwear itself, which all barefoot testing ignores.

    With the regard to Halstead and Redmond study, one has to be careful in intepretation. What they actualy found was that a linear model did not fit the static versus dynamic raw data well. This is not necessarilly the same as "no association". Think about it: how many stress-strain curves for biological tissues or biological structures do you see that are perfectly linear? How much variation is there likely to be in the stress/ strain curve for hallux dorsiflexion between individuals? Is it surprising then that the deformation occurring in response to the variable force being applied by the hands of the observers to the various 1st MTPJ's of the subjects in the static part of the Halstead and Redmond study did not correlate linearly with the deformation produced by the much larger variable forces being applied to the hallux of the subjects during dynamic function? I should think it's a no brainer that it wouldn't be a linear relationship given that the loading was not standardised in either test condition and what we know about the stress/strain relationships of biological visco-elastic structures; for starters they're visco-elastic- so rate of loading is important too- right? Throw in the variability between subjects and you are never going to see a linear model fit their data. Yet that is what the study tested.

    Lucy, when you said: "The change in weight-bearing resistance when the foot is tested on an orthosis is impressive, but if there's no relation between that and real walking.." I'm sure you realise that the study you cited didn't actually measure "resistance", so we cannot tell whether "weight-bearing resistance" (I assume you mean some qualitative feel of stiffness) has any relation with "real walking" on the basis of that study.

    Really we need dynamic, in-shoe measurement of hallux dorsiflexion stiffness- all yours, Jo.
  6. jpaton

    jpaton Welcome New Poster

    Re: FHL - old school or too important to miss

    Thanks for your thoughts and interest.

    I really like the idea of measuring hallux dorsiflexion stiffness, this measure could be particularly relevant to our target population.

    Unfortuataly I suspect we would be limited to developing a static measure without footwear- a small step in the right direction dont you think.

    Will let you know what we come up with.

    Best wishes

  7. Re: FHL - old school or too important to miss

    And the variation in terrain and the variation in activities of daily living which the laboratory testing of flat level walking ignores too. Life ain't like that.
  8. Re: FHL - old school or too important to miss

    I'd measure it as a radial deformation with a method of standardising the lever arm twixt subjects with a good quality load cell. I'd use a stepper motor through something like an Arduino board to standardise rate of loading. Pretty simple jig to build for the engineering bod's at the Uni.
  9. efuller

    efuller MVP

    Re: FHL - old school or too important to miss

    I'm not expecting Functional Hallux Limitus (FnHL) to be one of the larger factors in falls. I'd expect muscle weakness to be a much bigger factor. There is also an ethical issue of not giving someone with a foot drop an AFO. (Should take a quick look and see if dorsiflexion assisst AFO vs falls has been done)

  10. Hi Joanne:

    There have been some good answers already to your question. Functional hallux limitus (FnHL) is, by definition, a dynamic entity, with a lack of dorsiflexion of the hallux occurring while weightbearing even though the hallux can easily dorsiflex when the foot is not bearing weight. I agree with Eric in that I doubt that FnHL would be a specific cause of significant gait instability. However, I do also think that looking at the presence or absence of FnHL in post-stroke patients may be helpful at seeing how these patients can best be treated.

    Also, Simon's point about measuring hallux dorsiflexion stiffness is another good idea since the load vs deformation characteristics of hallux dorsiflexion would best measure the mechanical dysfunction that causes FnHL. However, measuring hallux dorsiflexion stiffness accurately may be difficult unless a specialized rig was constructed.

    Why not have a compromise measure? First measure the range of hallux dorsiflexion in a non-weightbearing situation to see if they have a structural hallux limitus or not and also measure the hallux dorsiflexion in bipedal standing and by hooking up a digital weighing scale (like a fish scale) to a strap that could be centered around the hallux IPJ and determine how much tension force at the hallux IPJ is required to dorsiflex the hallux 20 degrees, for example (if that range is possilbe in the non-weightbearing situation).

    This should be fairly easy to measure and would give you at least one load vs deformation measurement for hallux dorsiflexion in a weightbearing situation.

    Good luck!
  11. efuller

    efuller MVP

    Agreed. FnHL may not be a contributer to gait instability. However, if there is muscle weakness post stroke, there may be increased foot pathology related to FnHL. So, I agree it is one of those things on the long list of things to be studied. The problem is deciding which of those things on the list are most important so that the list can be narrowed to make a manageable study.

  12. Hi all!

    Everytime I read you, the seminar in Zaragoza comes to my mind! :D

    About FHL, in my humble opinion, it is still somehow a mystery, but some explanations seem to be arising, such its relationship with the first metatarsal mobility (first ray, actually) and foot pronation [Hild et al_Evaluation and biomechanics of the first ray in the patient with limited motion. Munuera_Effects of rearfoot-controlling orthotic treatment on dorsiflexion of the hallux in feet with abnormal subtalar pronation: a preliminary report]. An interesting post can be read in "podiatry today", summarising some concepts on HL (http://www.podiatrytoday.com/article/7486).

    About the study, Joanne, steps must be done, sometimes longer, sometimes shorter, sometimes jumping! Steps, non stop! :dizzy:

    I totally agree that a clinical testing with no objective tools can introduce a variability that may reduce the strength of the results. Dr. Kirby's idea of a scale to measure the force in weightbearing seems interesting to me; and how about a handheld dynamometer for non-weightbearing? [​IMG].

    Hope this post helps, and that I made myself clear, since English is not my mother tongue!
    Thanks for all the information we share in this arena!

    Carles Escalona PhD.
    Sport Science | Physiotherapy | Podiatry
  13. efuller

    efuller MVP

    Hello Carlos. I really enjoyed Zaragosa.

    I don't feel that Functional Hallux Limitus (FnHL) is that much of a mystery. In my windlass paper I described how STJ pronation is part of the arch lowering effect of the windlass.

    From the podiatry today article linked above
    Two points. An axis is an imaginary line and it cannot limit motion as they were hypothesizing above. So, that is not the reason.
    I do agree with the "foot types" that can cause high loads under the first met. However, the problem is not the foot types, but it is the high load under the first met. In my windlass paper I describe how when the ground pushes the met up, something in the foot has to hold it down. One of the things that holds it down is tension in the plantar fascia. High tension in the plantar fascia will limit hallux dorsiflexion. So, I don't see functional hallux limitus as that much of a mystery. In feet with functional hallux liimitus you can palpate the arch and feet that the fascia is tight.

  14. Hi Eric,
    sorry for late reply, I read it and it was very helpful! For me, now the mystery remains regarding "simple hoover cord maneuver that releases the tenodesis" proposed by Vallotton et al. [http://www.ncbi.nlm.nih.gov/pubmed/20479455] on JAPMA, 2010.
    Any idea on it?
    Thanks heaps!
  15. efuller

    efuller MVP

    I don't have a copy of the paper at hand. I think that I read the paper and I do recall the idea of FnHL being caused by FHL. I also recall not liking the idea, but I'm having a hard time remembering why I did not like the idea.

    I have a problem with this: " As a result, the mechanical support and stability mechanisms of the foot are disrupted, with important consequences during gait."
    The term stability mechanisms is another way of saying I have no idea what's going on. They might be able to define stability mechanims, but terms like that usually are an attempt to hide ignorance.

    Theoretically, tension in FHL tendon will create a plantar flexion moment at the mpj and that could prevent dorsiflexion of the hallux in gait. However, the tendon will also create a plantar flexion momenet at the IPJ. When there is a lot of activity of the FHL muscle, you will often see a hallux hammer toe from plantar flexion of the IPJ. (with your foot on the ground, use your FHL muscle to push your toe into the ground. You will often see plantar flexion of the IPJ when you do this.) So, if this "trapping" of the tendon near the ankle joint occurs, you would expect to see some plantar flexion of the IPJ some of the time.

    A tendon that gets "trapped" would not be an evolutionary advantage. I can't think of another tendon in the body where a similar thing happens. If the tendon were going to get trapped, a more likely location is where it passes under the 1st met head. At that location, it is being stepped on. The forces needed to trap the tendon would have to be huge. The forces attempting to dorsiflex the hallux at heel off are quite large. Why wouldn't the tendon break through the adhesions? Why do these alleged adhesions form?

    When you look at feet with functional hallux limitus, in stance, you can palpate the tension increase in the plantar fascia when you attempt to dorsiflex the hallux.

    So, to explain functional hallux limitus, you have to explain where a large plantar flexion moment of the MPJ can come from. I can concede that the FHL tendon, might theoretically cause it. However, I am doubtful that the EHL tendon is the cause.

  16. Dananberg

    Dananberg Active Member

    Hi Guys,

    Couldn’t resist. Eric wrote “In the foot with the medially positioned STJ axis, there will tend to be a high pronation moment from the ground.”

    Howard questions…..considering that we have all agreed that pathologic pronation occurs in the latter portion of single support, and pronation must be a manifestation of force dissipation. then please explain the following. Since the weight under the heel is rapidly DECREASING (or even 0 if the heel is off the floor) at this precise time, what causing a simultaneous increase in visible pronation?
    On to the discussion at hand. Joanne, FnHL can and does cause disturbances in geriatric gait, stroke or not. In a private industry oxygen uptake study, shoes constructed with a new patented sub 1st met relief designed specifically to manage FnHL, subjects averaged 9% fewer steps over a 20 minute test and used 9% less oxygen, all the while walking faster. 20 subjects were evaluated so there was little doubt that this was effective.

    The faster you walk, the steadier you become. This is known as resonant pace. Commenting that FnHL is of no value in understanding instability is a gross injustice to patients, and unacceptably underestimates the FnHL effect on gait and posture. When you are functioning at the end of your capacity as with post CVA patients, this 9% can be huge. As speed and stability are integrally related, any treatment introduction which improves pace will simultaneously restore balance . Adding 1st ray cutouts to an orthotic Rx and/or other forms of 1st MTPJ mobilization methods are of incredible value in this patient population. In fact, if these patients have AFO’s, try cutting the foot plate back to end behind the met heads and add a 1st cutout. They will be amazed how the arch pressure IMMEDIATELY is relieved and how much easier it is to walk. I performed this countless times while in practice, and the results were always highly positive to the patient and very rewarding to me.

  17. efuller

    efuller MVP

    It is possible to have pathologic pronation at any point in stance. Initial pronation can be patholgic as well. I would argue that high initial pronation moment is the "pathologic" pronation in PT dysfunction. I would agree that pronation in late stance phase, around heel off, can also be pathologic.

    We disagree on whether "force dissipation" must be a cause of pronation. I would say that a pronation moment is the cause of pronation. It is important to identify the source of pronation moment if you are going to treat pronation. There is more than one possible source of pronation moment. You can have a pronation moment from ground reaction force when the center of pressure is lateral to the STJ axis. You can also have a pronation moment from muscular action. I would bet that at least some of the pronation that you see around heel off is muscular pronation. There are feet that exhibit initial pronation just after heel contact and then pronation stops. Then in midstance it starts again. When the pronation stopped right after contact, equilibrium was achieved in a position where there is further pronation range of motion available. Feet that can achieve equilibrium in a position that is not maximally pronated will tend to have more laterally deviated STJ axes. As gait approaches heel off, increased tension in the Achilles tendon will create a supination moment. This supination moment must be counteracted by a pronation moment from some source if the foot is to be prevented from going into the "sprained ankle" position. A likely source for this pronation moment is the peroneal muscles. This is what I beleive will cause at least some of the late stance phase pronation that is seen. This "muscle caused" pronation, is treated with a forefoot valgus wedge. A rearfoot varus heel wedge can make this pronation worse.

  18. I'll add my two cents also.

    First of all, subtalar joint (STJ) pronation during gait is not the result of "force dissipation" (Howard, please define "force dissipation" since I don't know what that means). Rather, very simply, STJ pronation is the result of the summation of all the STJ pronation moments acting on the foot being greater than the summation of all the STJ supination moments acting on the foot at any instant in time during gait. A net pronation moment acting across the STJ will cause STJ pronation to occur. A net supination moment acting across the STJ will cause STJ supination to occur. This is a basic application of the physics concept of rotational equilibrium.

    STJ pronation and supination moments may be either external, meaning caused by forces which act from outside the body, or they may be internal, meaning acting from within the body.

    An example of an external STJ pronation moment would be ground reaction force (GRF) acting vertically upward on the 5th metatarsal head lateral to the STJ axis. An example of an external STJ supination moment would be ground reaction force (GRF) acting vertically upward on the medial aspect of the plantar calcaneus medial to the STJ axis.

    An example of an internal STJ pronation moment would be contractile activity of the peroneus brevis muscle. Since this peroneus brevis muscle tension force acts within the body on an internal structure (i.e. 5th metatarsal base) it would be considered an internal force causing an internal STJ pronation moment. An example of an internal STJ supination moment would be contractile activity of the posterior tibial muscle. Since this posterior tibial muscle tension force acts within the body on an internal structure (i.e. navicular tuberosity), it would be considered an internal force causing an internal STJ supination moment.

    Now, more specifically to Howard's statement, just because GRF under the heel is decreasing in late midstance, this does not mean there are no sources for increased STJ internal or external pronation moments during late midstance. In most instances of patients with late midstance pronation, there is a medially deviated STJ axis which, when the forefoot is subjected to increased GRF during late midstance, will cause an increase in external STJ pronation moment and an increase in STJ pronation motion (see illustration below). However, as Eric noted, late midstance pronation may also occur in feet with normal to lateral STJ axis location since if the central nervous system determines that excessive STJ supination moments may occur during late midstance, and an inversion ankle injury may result, it will increase the efferent neural activity to the peroneal muscles to prevent lateral ankle injury. The resultant increase in peroneal muscle contractile activity will generate an internal STJ pronation moment and also result in STJ pronation motion during late midstance.

    This is all a quite straight forward application of Newton's Laws of Motion and how they can be used to better understand why pronation and supination motions occur, and also why they don't occur, within the human foot during weightbearing and non-weightbearing activities.
  19. Dananberg

    Dananberg Active Member


    Ok, we at least agree that there must exist a timely “pronation moment” for late phase patho-mechanical function to exist. But the timing of this moment must coincide with the event. Any pronation which relates to the force moment of impact is far too early to produce the pathomechanical event which occurs far later in the cycle. Once peak heel load is reached, weight under the calcaneus decreases until heel off occurs. It stretches the imagination that decreasing force load can produce an increasing force moment. Some other source must be involved.

    You describe how increased tension in the Achilles will produce a supination moment, but this only equates with heel off. Should Achilles tension increase and heel off be delayed or fail to occur during single support phase, then it instead instigates a pronation moment and would time with what the later phase patho-mechanical event. Peroneal function can and does create pronation moments, but considering the relatively short ROM of a contracting peroneal group, and that the known predominate action of peroneal function is eccentric, then this argument fails to convince as a source of pathology. (Unless, of course, posterior tibial is dysfunctional or ruptured, and the peroneal induced moment is unopposed. In this case, heel lift also fails as evidenced by the clinical test of the absence of a single sided heel raise in PTTD or rupture.) Instead, focusing on the forefoot fulcrum point (ie, metatarsal heads) which provides mechanical advantage (2nd class leverage) to raise body weight and provide simultaneous re-supination during single support phase, provides insight into the process. Your published writings on windlass function clearly provide adequate explanation for re-supination, but windlass action is dependent on normal MTPJ function. And, as I have written countless times, failure here (ie, FnHL) creates a solid match to well-known temporal and mechanical events.

    The essential occurrence of lifting body weight over the last half of single support phase is crux of the matter. The classic double hump force/time curve depicts the rising and falling of body weight during the step. Reaching the 2nd peak in forefoot load requires efficiently managing the weight load associated with single support phase. This is provided by the foot’s ability to manage the following are all dependent on normal MTPJ function:
    • Permitting the CoM to advance forward beyond the weight bearing foot
    • To provide a leveraged fulcrum to lift body weight
    • To self-stabilize via windlass function
    • To minimize concentric and maximize eccentric muscular activity and therefore achieve peak gait efficiency.

    Failure of 1st MTPJ function would lead to a breakdown in the above process and create the events associated with late phase pronation. Why this occurs is clearly open to intense debate, but the fact that failure provides a reasonable answer as to timing and force utilization in the pathologic pronation process brings clarity to complex issue.

  20. efuller

    efuller MVP

    I just want to make sure that we are using the same terminology. For me, moment = torque. Reading your paragraph above it seems you could be using moment as a point in time. Is this why I'm confused by your term "force moment of impact?" I would agree that when pronation occurs the pronation moment (torque) must be present.

    Perhaps my explanation of equinus paradox can help you understand how as the heel lifts there can an increased pronation moment from the ground. The equinus paradox is that the Achilles tendon is a strong supinator of the STJ non weight bearing. Yet, we see feet with an equinus that pronate in response to the early heel off. We also see feet, more rarely, that supinate in response to the early heel off. (Root Orien and Weed have too separate sections in Normal, Abnormal Function of the Foot on this. One section is how an equinus causes supination and the other section is on how equinus causes pronation. The sections are right next to each other in the index, but in different sections of the book.) So, you have to be able to explain why you can see both pronation and supination with an equinus. The answer lies in looking at STJ axis position. The Achilles is a strong supinator. It is an even better plantar flexor of the ankle. It has a longer lever arm on the ankle joint as compared to the STJ. As the old Hicks paper shows, tension in the Achilles tendon shifts the balance point (=center of pressure) anteriorly and a little bit laterally. Hicks also showed that the balance point with no tendon tension was directly beneath the ankle and STJ axes. When muscles contract the balance point is shifted. With a medially deviated STJ axis foot, when the center of pressure is moved anteriorly, the center of pressure of ground reaction force will be farther lateral than in an average axis foot. Thus there will be a greater pronation moment from the ground in the medial STJ axis foot. Conversely, with a lateral STJ axis, the anterior shift of the center of pressure, there will be very little pronation moment from the ground, and you can see supination of the STJ. This is how you can explain the observation that you can see both pronation and supination with an equinus. There is still torque from ground reaction force at the STJ after heel lift.

    I don't understand your comment about short range of motion of the peroneal group. When you test these muscles they can produce a pronation moment/torque every where in the physiologic range of motion of the STJ. The muscles will create this torque eccentrically and concentrically. When you measure them during they may function eccentrically most of the time, but they are quite capable of functioning concentrically. I would argue that they will function as the person needs them to function for the task at hand. If someone has learned that they will sprain there ankle if they don't fire them to create a pronation motion right around heel off, they will choose to fire them, concentrically, to make the STJ pronate. Feet with lateral STJ axes will have different peroneal function than feet with medial STJ axes, because they have different needs to complete the same task.

    This is where we have disagreed in the past. I believe that the windlass is the cause of "abnormal" 1st MPJ function. I think that you believe that dysfunction of the MTPJ causes windlass dysfunction. I once asked you, what causes the MPJ to have dysfunction. You replied with a long list of things that I could explain with my version. For example, first ray is dorsiflexed by ground reaction force. When the first ray is dorsiflexed, the plantar fascia will become tighter and this creates the plantar flexion moment/torque that prevents the hallux from dorsiflexing. We agree on the events. We disagree on cause and effect.

    The pronation moment from the peroneal muscles, at the STJ, is strong enough to overcome the supination moment from the supination moment created by the windlass mechanism. The pronation moment from ground reaction force could also be strong enough to overcome the supination moment from the windlass mechanism. There are two different sources of pronation moment that can be large enough to make the windlass act in reverse and plantar create a plantar flexion moment on the hallux. They need to be treated differently.

    We agree on the observations. We probably would agree on the orthotic design for a certain condition. Where we disagree is on the explanations of why that orthotic would work and why those observations happen. It is indeed an interesting and complex issue.

  21. Dananberg

    Dananberg Active Member

    Eric wrote: “The equinus paradox is that the Achilles tendon is a strong supinator of the STJ non weight bearing. Yet, we see feet with an equinus that pronate in response to the early heel off. We also see feet, more rarely, that supinate in response to the early heel off.”

    To which Howard replies: Eric, I can make the exact same case for FnHL causing (or if not present, not causing) pronation related to equinus. Equinus was discussed as a major influence on foot function during my Pod School days. I was taught that the midfoot compensated for the presence of equinus, and this was why children with equinus could not be placed in rigid, neutral orthotics. I could never understand what they were compensating for, and why they didn’t bounce off the orthotics at heel lift. The answer was FnHL. Nothing else made sense to me. If present, then even with early heel lift, a retrograde pronation occurs as the early heel lift without MTPJ motion caused the midfoot’s pronatory response.

    Eric continued: “When muscles contract the balance point is shifted. With a medially deviated STJ axis foot, when the center of pressure is moved anteriorly, the center of pressure of ground reaction force will be farther lateral than in an average axis foot.”

    I would agree that as tension develops within the Achilles, the balance point shifts anteriorly, but, I would add, not all the way to the forefoot. For efficient forward weight transfer and balance point development, the metatarsals must rotate thru the sagittal plane, moving their bases about the pivotal heads. Without this motion, the ability to transfer load to the osseous structures of the forefoot is lost, and soft tissue must instead manage the load. Over time and plastic deformation, we see that result; a pronated foot appearing as a primary issue when it is the result of stress over time.

    Now, returning to the question that Joanne originally raised, it is the clinical manifestation of FnHL in the geriatric community is one that is often ignored. I treated countless geriatrics for gait and balance issues over my practice years, and was consistently pleased with the outcome provided by simply releasing the 1st MTP joint. To say that this can be ignored because it does not fit a paradigm misses the elegance of the body in motion.


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