The banana hallux. When the big toe curls upward

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Note: over-extension of the hallux and over-flexion of the 2nd toe. How can they both be so different at rest ? read on

This is common, but not commonly addressed. And, it can become a cause of symptoms.
Note how curled up into extension the hallux appears. This is just a representation of hyperextension of the distal phalange at the IP joint (interphalangeal joint).
This often occurs in hallux limitus/rigidus, where there is insufficient extension through the 1st MTP joint (metatarsophalangeal joint). In that condition, they client attempts to toe off, needing extension (dorsiflexion) at that joint, and they do not have it, so the extension can be found through arch collapse (1st metatarsal dorsiflexion) or through extension at the IP joint. Over time, form follows function and you will often see this presentation.

However, we do not need to see impaired ROM function at the 1st MTP joint, as in this case. This foot had full 1st MTP ROMs.
In this case, this toe represented massive imbalance between the long and short flexors and extensors. Specifically, increased use and strength in the EHL (extensor hallucis longus) and weakness and unawareness of how to even engage the short extensor (EHB).
Similarly, the pairing met the one we always see with this, that being weak and even difficulty of awareness to engage the FHL (flexor hallucis longus) and over-activity of the FHB (short flexor-flexor hallucis brevis).
There pairings: weak: EHB and FHL & overactive: EHL and FHB over time will result in this presentation.

In gait, you will note poor compentence and purchase of the hallux on the ground and thus a sharing of that load through overflexion hammering of the 2nd digit through increased FDL activity (note the great evidence of this with the thick obvious callus at the tip of the 2nd toe).
These clients can also often have pain at the plantar aspect of the Metatarsal head because of sesamoid imbalanced loading (sesamoiditis) as well as frank pain at the MTP joint dorsally or plantarward. One will often note a medial pinch callus on these feet medial to the metatarsal head, from a rotational spin toe off. Hallux valgus and bunion formation are also not uncommmon at all in this incompetent hallux presentation.
PS: the solution is so much more complex and involved than just towel-scrunches and marble pick up games. I mean, come on, we can do better that this team !
This requires some serious reteaching of how to use the foot, arch, tripod, windlass and foot-ground engagement skills.

Shawn and Ivo, the gait guys

#gait, #gaitproblems, #gaitcompensatins, #gaitanalysis, #bunions, #halluxvalgus, #sesamoiditis, #turftoe, #halluxlimitus, #pinchcallus, #bananatoe, #metatarsalgia, #thegaitguys, #hammertoe

Premature heel rise: Part 2

VIDEO: an atypical case of Premature heel rise. A follow up video for yesterdays discussion on the topic.

You should easily see premature heel rise here in this video. We will discuss this case at length with other video projections on our Patreon site next week, if you wish to dive further.

But here you should see, lets focus on the right limb, premature heel rise (again, stick with just watching the right foot/leg). This is, in-part, because this person does not achieve adequate hip extension, you should clearly be able to see that. Loss of terminal hip extension means premature heel rise, no exceptions. Train your eye to see this, you do not need expensive video software to see this.

So, Why inadequate hip extension? Well, just look at the amount of right knee flexion going into terminal stance, it is still heavily flexed and this forces them to prematurely heel rise, avoiding terminal hip extension, and prematurely load the forefoot. Without a knee that extends sufficiently, the hip cannot extend sufficiently, and thus premature heel rise is inevitable. And, trying to solve this issue down at the foot/ankle level is foolish in this case. Stretching this calf day after day until aliens come visit earth will still not be enough stretch time to fix this premature heel rise (ie. get that heel to stay down longer). There is a good reason why this is happening in this person, and it is a neurologic one, one we will discuss on the Patreon site for our Patrons. And, the reason does not matter for the concept I am teaching here today.

For today, you need to be able to see premature heel rise, and know all of the issues behind it, including causes, so that you can direct your phyiscial examination to solve your client's puzzle.
I have included yesterday's post below so you can review and bring this further together.
This is the kind of stuff we will do at Dr. Allen's Friday night Gait Lab, over some beverages. A unique, clinically curious and hungry 25 people need only apply. If you want to get to the next level of your human movement game, this is a way to get there.

Yesterday's post: We know that early/premature heel rise (PHR) leads to premature loading of the forefoot.
We know that premature heel rise (PHR) speeds us through many of the timely mechanical events that need and should occur for to get to safe and effective toe off during walking and running gaits.
This is why there are so many variables that need to be assessed and checked before instituting care to address the premature heel rise, because many times the problem is not even near the heel.
Consider, examine, assess (this is not an exhaustive list either) of causes of PHR
-short calf complex
-short quad (limits hip extension)
- short hip flexors
-anterior pelvis tilt as one's deviated norm posture
- prolonged or excessive rearfoot inversion
-lack of appropriate pronation (sustained supination)
-hallux limitus, rigidus
- weak anterior compartment lower leg
-lack of hip extension/weak glutes
-knee flexion contracture
- neurologic (toe walking gait from youth)
-painful achilles tendon mechanism
- loss of ankle rocker (which has its own long list)
. . . . to name a few

This is why you need to examine your clients, even after a gait analysis. Because, as we like to say, what you see is not your clients gait problem, it is their work around to other mechanical deficits.
After all, telling someone they just need to lengthen/stretch their calf to keep that heel down longer is utterly foolish.

*want to learn more about this stuff, you can join the upcoming Dr. Allen, Friday night Gait Lab series that he will be having in his office one Friday a month, in his Chicagoland office. Stay tuned for that notice. I will take only 25 people per session. We will dive into videos, cases, concepts, white-board rabbit holes, and enjoy some beverages and learn together. Stay tuned. The first 25 to pay and sign up are in !

Shawn Allen, the other gait guy

#gait, #gaitproblems, #gaitanalysis, #heelrise, #PHR, #prematureheelrise, #achilles, #achillestendinitis, #anklerocker, #heelrocker, #forefootpain, #halluxlimitus, #halluxrigidus, #heelpain

Premature heel rise: Part 1

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We know that early/premature heel rise (PHR) leads to premature loading of the forefoot.
We know that premature heel rise (PHR) speeds us through many of the timely mechanical events that need and should occur for to get to safe and effective toe off during walking and running gaits.
This is why there are so many variables that need to be assessed and checked before instituting care to address the premature heel rise, because many times the problem is not even near the heel.
Consider, examine, assess (this is not an exhaustive list either) of causes of PHR
-short calf complex
-short quad (limits hip extension)
- short hip flexors
-anterior pelvis tilt as one's deviated norm posture
- prolonged or excessive rearfoot inversion
-lack of appropriate pronation (sustained supination)
-hallux limitus, rigidus
- weak anterior compartment lower leg
-lack of hip extension/weak glutes
-knee flexion contracture
- neurologic (toe walking gait from youth)
-painful achilles tendon mechanism
- loss of ankle rocker (which has its own long list)
. . . . to name a few

This is why you need to examine your clients, even after a gait analysis. Because, as we like to say, what you see is not your clients gait problem, it is their work around to other mechanical deficits.
After all, telling someone they just need to lengthen/stretch their calf to keep that heel down longer is utterly foolish.

*want to learn more about this stuff, you can join the upcoming Dr. Allen, Friday night Gait Lab series that he will be having in his office one Friday a month, in his Chicagoland office. Stay tuned for that notice. I will take only 25 people per session. We will dive into videos, cases, concepts, white-board rabbit holes, and enjoy some beverages and learn together. Stay tuned. The first 25 to pay and sign up are in !

Shawn Allen, the other gait guy

#gait, #gaitproblems, #gaitanalysis, #heelrise, #PHR, #prematureheelrise, #achilles, #achillestendinitis, #anklerocker, #heelrocker, #forefootpain, #halluxlimitus, #halluxrigidus, #heelpain

The “Standing on Glass” Static Foot/Pedograph... PART 2

The “Standing on Glass” Static Foot/Pedograph... PART 2
We hope you find this case presentation dialogue interesting.

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* note: This is a static assessment dialogue. One cannot, and must not, make clinical decisions from a static assessment. As in all assessments, information is taken in, digested and them MUST be confirmed, denied and/or at the very least, folded into a functional and clinically relevant assessment of the client before the findings are accepted, dismissed and acted upon.

Here is the case . . .

Part 2: “Standing on Glass” Static Foot/Pedograph Assessment

* note (see warning at bottom): This is a static assessment dialogue. One cannot, and must not, make clinical decisions from a static assessment. The right and left sides are indicated by the R and L circled in pink. There are 4 photos here today.

Blue lines: Last time we evaluated possible ideas on the ORANGE lines here, it would be to your advantage to start there.

We can see a few noteworthy things here in these photos. We have contrast-adjusted the photo so the pressure areas (BLUE) are more clearly noted. There appears to be more forefoot pressure on the right foot (the right foot is on the readers left), and more rearfoot pressure on the left (not only compare the whiteness factor but look at the displacement of the calcaneal fat pad (pink brackets). There is also noticeably more lateral forefoot pressure on the left. There is also more 3-5 hammering/flexion dominance pressure on the left. The metatarsal fat pad positioning (LIME DOTS represent the distal boundary) is intimately tied in with the proper lumbrical muscle function (link) and migrates forward toward the toes when the flexors/extensors and lumbricals are imbalanced. We can see this fat pad shift here (LIME DOTS). The 3-5 toes are clearly hammering via flexor dominance (LIME ARROWS), this is easily noted by visual absence of the toe shafts, we only see the toe pads. Now if you remember your anatomy, the long flexors of the toes (FDL) come across the foot at an angle (see photo). It is a major function of the lateral head of the Quadratus plantae (LQP) to reorient the pull of those lesser toe flexors to pull more towards the heel rather than on an angle. One can see that in the pressure photos that this muscle may be suspicious of weakness because the toes are crammed together and moving towards the big toe because of the change in FDL pull vector (YELLOW LINES). They are especially crowding out the 2nd toe as one can see, but this can also be from weakness in the big toe, a topic for another time. One can easily see that these component weaknesses have allowed the metatarsal fat pad to migrate forward. All of this, plus the lateral shift weight bearing has widened the forefoot on the left, go ahead, measure it. So, is this person merely weight bearing laterally because they are supinating ? Well, if you read yesterday’s blog post we postulated thoughts on this foot possibly being the pronated one because of its increased heel-toe and heel-ball length. So which is it ? A pronated yet lateral weight bearing foot or a normal foot with more lateral weight bearing because of the local foot weaknesses we just discussed ? Or is it something else ? Is the problem higher up, meaning, are they left lateral weight bearing shift because of a left drifted pelvis from weak glute medius/abdominal obliques ? Only a competent clinical examination will enlighten us.

Is the compensation top-down or bottom up, or both in a feedback cycle trying to find sufficient stability and mobility ? These are all viable possibilities and you must have these things flowing freely through your head during the clinical examination as you rule in/rule out your hands-on findings. Remember, just going by a screen to drive prescription exercises from what you see on the movement screen is not going to necessarily fix the problem, it could in fact lead one to drive a deeper compensation pattern.

Remember this critical fact. After an injury or a long standing problem, muscles and motor patterns jobs are to stabilize and manage loads (stability and mobility) for adequate and necessary movement. Injuries leave a mark on the system as a whole because adaptation was necessary during the initial healing phase. This usually spills over during the early movement re-introduction phase, particularly if movement is reintroduced too early or too aggressively. Plasticity is the culprit. Just because the injury has come and gone does not mean that new patterns of skill, endurance, strength (S.E.S -our favorite mnemonic), stability and mobility were not subsequently built onto the apparently trivial remnants of the injury. There is nothing trivial if it is abnormal. The forces must, and will, play out somewhere in the body and this is often where pain or injury occurs but it is rarely where the underlying problem lives.

Come back tomorrow. We will try to bring this whole thing together, but remember, it will just be a theory for without an exam one cannot prove which issues are true culprits and which are compensations. Remember, what you see is often the compensatory illusion, it is the person moving with the parts that are working and compensating not the parts that are on vacation. See you tomorrow friends !

Shawn and ivo, the gait guys

* note: This is a static assessment dialogue. One cannot, and must not, make clinical decisions from a static assessment. As in all assessments, information is taken in, digested and then MUST be confirmed, denied and/or at the very least, folded into a functional and clinically relevant assessment of the client before the findings are accepted, dismissed and acted upon. As we always say, a gait analysis or static pedograph-type assessment (standing force plate) is never enough to make decisions on treatment to resolve problems and injuries. What is seen and represented on either are the client’s strategies around clinical problems or compensations. Today’s photo and blog post are an exercise in critical clinical thinking to get the juices flowing and to get the observer thinking about the client’s presentation and to help open up the field to questions the observer should be entertaining. The big questions should be, “why do i see this, what could be causing these observances ?”right foot supinated ? or more rear and lateral foot……avoiding pronation ?


Walking and Running Require Greater Effort from the Ankle than the Knee Extensor Muscles.

Attached is an older video from a few years back , it is very similar in execution to the heel-rise ball squeeze exercise which is the precursor to this more functional engagement as shown in this video today.

The important premise is that you have to have command of the entire posterior compartment if you are to get safe, effective, efficient and adequate ankle plantarflexion. As we have discussed many times, if you do not have the requisite skills as shown in this video you are in trouble and ankle sprains and other functional pathologies are not unlikely to visit you. Additionally, without requisite posterior compartment endurance and an ability to engage what I like to refer to as "top end" strength in the heel rise is an asymmetrial loading issue and can lead to compensatory adaptations up the kinetic chain. Make no mistake, the load will go somewhere, and thus the work will be done somewhere. In this video you should be able to clearly see and understand that one must be able to achieve top end posturing and have command of lateral and medial forefoot loading responses and challenges if clean forward function and power is to be achieved, and injuries from extremes of motion medially and laterally are to be avoided. Furthermore, as eluded to here and in several of our podcasts (and in the study included below), an inability to achieve top end posturing will lead to changes in forefoot loading, may spill over into endurance challenges prematurely in the posterior mechanism, and create changes in the timing of the gait cycle (things like premature or delayed heel rise, premature or delayed forefoot loading, recruitment of other components of the posterior chain just to name a few). This parsing and sharing of loads and responsibilities is laid out in the Kulmala study referenced today. The study could be extrapolated to say, I believe, that particularly in sprinting, a failure to achieve top end heel rise through effective posterior mechanism contraction, will change the load sharing between the posterior compartment and the quadriceps. After all, if the calf is weak, the ankle is not in as much plantarflexion, this could mean more knee flexion and thus raise demands on the quadriceps, logically changing knee mechanics. This is exactly why we spend so much time at every patient visit looking for full range of motion at the joints and then determine the skill, endurance and strength of the associated muscles in supporting that range. Then, of course, comparing this function to the opposite limb. Symmetry is not everything, but it is definitely a major factor in safe efficient and injury free locomotion.

* Please give great thought to the part in the video where I discuss the drop phase in jumping. All too often we at looking for the propulsive mechanics and forget that a failure there will also be represented during the adaptive phase. Ankle sprains rarely occur from propulsive pushing off, they occur from a failure to properly reacquaint the foot to the ground on the following step.
-Dr. Shawn Allen, one of the gait guys.

In this study the authors noted:
"During walking, the relative effort of the ankle extensors was almost two times greater compared with the knee extensors. Changing walking to running decreased the difference in the relative effort between the extensor muscle groups, but still, the ankle extensors operated at a 25% greater level than the knee extensors. At top speed sprinting, the ankle extensors reached their maximum operating level, whereas the knee extensors still worked well below their limits, showing a 25% lower relative effort compared with the ankle extensors."

And concluded that:
"Regardless of the mode of locomotion, humans operate at a much greater relative effort at the ankle than knee extensor muscles. As a consequence, the great demand on ankle extensors may be a key biomechanical factor limiting our locomotor ability and influencing the way we locomote and adapt to accommodate compromised neuromuscular system function."

Med Sci Sports Exerc. 2016 Nov;48(11):2181-2189. Walking and Running Require Greater Effort from the Ankle than the Knee Extensor Muscles. Kulmala JP1, Korhonen MT, Ruggiero L, Kuitunen S, Suominen H, Heinonen A, Mikkola A, Avela J.
https://www.ncbi.nlm.nih.gov/pubmed/27327033

https://youtu.be/8T9UzOaYxmo

the gait guys
#gait, #gaitproblems, #thegaitguys, #gaitanalysis, #heelrise, #calfstrength, #toeoff, #forefootloading, #metatarsalgia, #inversionsprain


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Pincher nails.  Who knew !?

Written by Dr. Shawn Allen

*note: there are two photos here in today’s blog post, look for the side scroll arrows and click on the small box in the upper left corner if you cannot see the photo

 We have seen this one for years in our clinics but we never got around to researching it and pondering the condition more deeply.  Here is our mantra for today, Form follows Function.

Studies seem to be undecided on the cause of this entity. Some suggest that pincer nails are caused by lack of upward mechanical forces on the toe pad where others remark that they can be observed amongst the healthy mechanical walkers. Hitomi’s study suggests that the affected toes fail to receive adequate physical stimulation from proper toe and forefoot loading. Please read on, this gets interesting.

According to Hitomi’s study, in both the barefoot and shod state,

“the pincer nail group had significantly lower pressure on the first toe than the control group. In both the barefoot and shod state, the peak pressure area was mostly the metatarsal head area in the pincer nail group, whereas it was mostly the first toe area in the control group. Binomial logistic regression analysis revealed that peak pressure area was a significant risk factor for pincer nail development.”

This seems to suggest that there is insufficient or aberrant use of downward pressure on the toes and into the toe pads. Hitomi speaks of the locale of the peak pressure, seemingly proposing from this study that it should not be under the metatarsal heads. This, in our experience and thinking, could suggest that more long flexor dominance is present. This long flexor activity seems to create some disfunction not only in the activity of the lumbrical muscles but also altered pressures in the metatarsal (MET) heads.  It certainly alters distal toe pressures which can alter skin and nail responses (see our blog post on subungal hematomas for more on this topic where we discuss principles of counter pressure and shear forces). We try to teach a “spread and reach with long flat toes” approach to our clients in correcting bad habits such as toe hammering and gripping (which are often a result of flawed biomechanics elsewhere).

The nail bed is very rich in vasculature (hence the cause of the dreaded hematoma, the black toenail) and nerve endings.  The nail bed is a derivative of the epidermis containing keratin which gives it its hard nature. The nail consists of the nail plate, the nail fold, the nail matrix, the sterile matrix and the hyponychium. There are many factors that go into the formation of a normal nail, including blood flow, nutrition, local neurogenic factors and not to forget, mechanical loading issues. Failure of any of these issues can lead to softening, brittle, thinning, diseased or malformed nails. The nail grows from a nail root in front of the cuticle and grows distally at a slow but (usually) steady rate.  It is interesting to note that the long extensor tendon (EDL) attachment is close to the proximal nail bed root area thus it brings forward thinking of possible imbalances between long and short flexors and extensor tendons/muscles and their patterns of imbalance in toe gripping and hammering that could cause a change in function which could drive a change in form.  We have all heard it, form follows function, why should this area be any different ?

Hitomi also mentioned something interesting in his study, the observation that bed ridden clients seem to have a predilection to pincer toes.  This at least seems to fit the aberrant loading patterns, in this case an absence of. The study also started some interesting thinking in us when it mentioned a hypothesis,

“that human nails are constitutively equipped with an automatic shrinkage function that allows them to adapt to daily upward mechanical forces.”

This was a fascinating hypothesis to us. It seems to make sense. If constant downward pressure on the toe pads were present, the toe nails would always be undergoing a flattening and spreading response so it could make sense that the nails have a built in curve and shrinkage function offsetting and adapting to the constant distorting pressures (the flattening and spreading forces).  Hence, some possible clarity in Hitomi’s hypothesis that pincer nails are caused by lack of (and in our thinking, distorted) upward mechanical forces on the toe pad.  And, when those distorting pressures are placed elsewhere (ie. the MET heads or tips of the toes as in our subungal hematoma hypothesis) or faulting gripping or hammering loading the automatic shrinkage function is left to dominate.

We think Hitomi’s hypothesis is correct. Here is why (this is paraphrased from our blog post on subungal hematomas and our revolutionary thinking on why they occur and it seems to fit well with pincer nail formation as well).

…  when the skin is pulled at a differential rate over the distal phalange (from gripping of the toes rather than downward pressing through the toe pad) there will be a net lifting response of the nail from its bed as the skin is drawn forward of the backward drawn phalange  (there is a NET movement of skin forward thus lifting the nail from its bedding).  For an at-home example of this, put your hand AND fingers flat on a table top. Now activate JUST your distal long finger flexors so that only the tip of the fingers are in contact with the table top (there will be a small lifting of the fingers). There should be minimal flexion of the distal fingers at this point. Note the spreading and flattening of the nail.  Now, without letting the finger tip-skin contact point move at all from the table, go ahead and increase your long flexor tone/pull fairly aggressively. You are in essence trying to pull the finger backward into flexion while leaving the skin pad in the same place on the table. Feel the pressure building under the distal tip of the finger nail as the skin is RELATIVELY drawn forward.]   This is fat pad and skin being drawn forward (relative to the phalange bone being drawn backward) into the apex of the nail. Could this be magnifying the curvature of the nail and not offsetting the “automatic curving and shrinkage” function of the nail ? We think it is quite possible.

So, there you have it. We will dive deeper on this topic another time, but after reading Hitomi’s study our brain’s started buzzing because we had discussed this process similarly a few years back in our Subungal Hematoma blog post.

And, if you are thinking about chronic repeated ingrown toe nails with this clinical entity, your thoughts are clearly on a logical path.  There is a correlation it seems.

And, as for the horrific metal bar correction you see in the other photo above, this too is new to our eyes.  It seems rather medieval, something one might see in the gallows of yesteryear.  And if that doesn’t curl your hair and make you nauseated, try looking at what this one guy did, a DIY remedy (caution, not for the feint of heart). https://www.mja.com.au/journal/2005/182/4/diy-pincer-nail-repair-brace-yourself

ShawnAllen, one of the gait guys

References:

Foot loading is different in people with and without pincer nails: a case control study  Hitomi Sano1*, Kaori Shionoya2 and Rei Ogawa1  Journal of Foot and Ankle Research 2015, 8:43

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Part 2: “Standing on Glass” Static Foot/Pedograph Assessment

* note (see warning at bottom): This is a static assessment dialogue. One cannot, and must not, make clinical decisions from a static assessment. The right and left sides are indicated by the R and L circled in pink. There are 4 photos here today.

Blue lines: Last time we evaluated possible ideas on the ORANGE lines here, it would be to your advantage to start there. 

We can see a few noteworthy things here in these photos. We have contrast-adjusted the photo so the pressure areas (BLUE) are more clearly noted. There appears to be more forefoot pressure on the right foot (the right foot is on the readers left), and more rearfoot pressure on the left (not only compare the whiteness factor but look at the displacement of the calcaneal fat pad (pink brackets). There is also noticeably more lateral forefoot pressure on the left. There is also more 3-5 hammering/flexion dominance pressure on the left.  The metatarsal fat pad positioning (LIME DOTS represent the distal boundary) is intimately tied in with the proper lumbrical muscle function  (link) and migrates forward toward the toes when the flexors/extensors and lumbricals are imbalanced. We can see this fat pad shift here (LIME DOTS). The 3-5 toes are clearly hammering via flexor dominance (LIME ARROWS), this is easily noted by visual absence of the toe shafts, we only see the toe pads. Now if you remember your anatomy, the long flexors of the toes (FDL) come across the foot at an angle (see photo). It is a major function of the lateral head of the Quadratus plantae (LQP) to reorient the pull of those lesser toe flexors to pull more towards the heel rather than on an angle. One can see that in the pressure photos that this muscle may be suspicious of weakness because the toes are crammed together and moving towards the big toe because of the change in FDL pull vector (YELLOW LINES). They are especially crowding out the 2nd toe as one can see, but this can also be from weakness in the big toe, a topic for another time. One can easily see that these component weaknesses have allowed the metatarsal fat pad to migrate forward. All of this, plus the lateral shift weight bearing has widened the forefoot on the left, go ahead, measure it. So, is this person merely weight bearing laterally because they are supinating ? Well, if you read yesterday’s blog post we postulated thoughts on this foot possibly being the pronated one because of its increased heel-toe and heel-ball length. So which is it ? A pronated yet lateral weight bearing foot  or a normal foot with more lateral weight bearing because of the local foot weaknesses we just discussed ? Or is it something else ? Is the problem higher up, meaning, are they left lateral weight bearing shift because of a left drifted pelvis from weak glute medius/abdominal obliques ?  Only a competent clinical examination will enlighten us.

Is the compensation top-down or bottom up, or both in a feedback cycle trying to find sufficient stability and mobility ? These are all viable possibilities and you must have these things flowing freely through your head during the clinical examination as you rule in/rule out your hands-on findings.  Remember, just going by a screen to drive prescription exercises from what you see on the movement screen is not going to necessarily fix the problem, it could in fact lead one to drive a deeper compensation pattern. 

Remember this critical fact.  After an injury or a long standing problem, muscles and motor patterns jobs are to stabilize and manage loads (stability and mobility) for adequate and necessary movement. Injuries leave a mark on the system as a whole because adaptation was necessary during the initial healing phase. This usually spills over during the early movement re-introduction phase, particularly if movement is reintroduced too early or too aggressively.  Plasticity is the culprit. Just because the injury has come and gone does not mean that new patterns of skill, endurance, strength (S.E.S -our favorite mnemonic), stability and mobility were not subsequently built onto the apparently trivial remnants of the injury.  There is nothing trivial if it is abnormal. The forces must, and will, play out somewhere in the body and this is often where pain or injury occurs but it is rarely where the underlying problem lives.

Come back tomorrow.  We will try to bring this whole thing together, but remember, it will just be a theory for without an exam one cannot prove which issues are true culprits and which are compensations. Remember, what you see is often the compensatory illusion, it is the person moving with the parts that are working and compensating not the parts that are on vacation.  See you tomorrow friends !

Shawn and ivo, the gait guys

* note: This is a static assessment dialogue. One cannot, and must not, make clinical decisions from a static assessment. As in all assessments, information is taken in, digested and then MUST be confirmed, denied and/or at the very least, folded into a functional and clinically relevant assessment of the client before the findings are accepted, dismissed and acted upon. As we always say, a gait analysis or static pedograph-type assessment (standing force plate) is never enough to make decisions on treatment to resolve problems and injuries. What is seen and represented on either are the client’s strategies around clinical problems or compensations.  Today’s photo and blog post are an exercise in critical clinical thinking to get the juices flowing and to get the observer thinking about the client’s presentation and to help open up the field to questions the observer should be entertaining.  The big questions should be, “why do i see this, what could be causing these observances ?”right foot supinated ? or more rear and lateral foot……avoiding pronation ?

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The case of the missing toes.

OK, a bit dramatic but as you can see in the plantar view above, all you can see is the toe pads, the rest of the digit shafts are hidden.  

This is a classic example of a foot imbalance. We have talked about this many times before but the attached video link here  ( http://youtu.be/IIyg7ejYNOg ) shows it very well.  Read on.

There is shortness and increased resting tone in the short toe extensors (EDB, extensor digitorum brevis) and long toe flexors (FDL=flexor dig. longus) with insufficiency in the short flexors and long extensors. This pairing creates a hammer toe effect.  In the video, you can see that these toes are showing early hammering characteristics, but not yet rigid ones. The key word there is, “yet” so this is still a correctable phenomenon at this point.  You can also clearly see the distal migration of the metatarsal fat pad. The fat pad has migrated forward of the MET heads and is being pulled forward by the excess tension in the long toe flexors. As this imbalance in the toe flexors and extensors develops, the forefoot mechanics get impaired and the lumbricals (which anchor off off the FDL) become challenged. Their contributory biomechanics, amongst other things, help to keep the fat pad in place under the metatarsal heads. You can see in this video link above that by proximally migrating (towards the heel) just the fat pad back under the MET heads the resting mechanics of the toes changes, for the better.  

Remember the other functions of the lumbricals ?  their other major functions, namely: thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

Here is another blog post we did on a similar presentation.http://thegaitguys.tumblr.com/post/14766494068/a-case-of-plantar-foot-pain-during-gait-this

Proper balance of the toe flexors and extensors, and their harmony with lumbricals and fat pad amongst other things will give healthy long flat toes that can help the proximal biomechanics of the foot.  If you have neuromas, metatarsalgia, hammer toes, claw toes, migrating toes, bunions or hallux valgus amongst many other things, this might be a good place to start.   

There are exercises that can help this presentation, but understanding “the why” is the first step.

Shawn and Ivo

The Gait Guys

Pod 43. Achilles problems, Neurology of watching sports, PEDS, hip joint centration.

Pod 43. Achilles problems, Neurology of watching sports, PEDS, hip joint centration, risks of swaddling babies and so much more. Join us today for this great podcast !

A. Link to our server:

http://thegaitguys.libsyn.com/podcast-43-achilles-problems-neurology-of-watching-sports-peds-hip-joint-centration-risks-of-swaddling-babies-and-so-much-more-join-us-today-for-this-great-podcastB.

iTunes link:

https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138

C. Gait Guys online /download store (National Shoe Fit Certification and more !) :

http://store.payloadz.com/results/results.aspx?m=80204

D. other web based Gait Guys lectures:

www.onlinece.com   type in Dr. Waerlop or Dr. Allen,  ”Biomechanics”

________________________________________

* Today’s show notes:

Neuroscience pieces:
1. Brief Exposure to Performance-Enhancing Drugs May Be Permanently ‘Remembered’ by Muscles
 
 Brief exposure to anabolic steroids may have long lasting, possibly permanent, performance-enhancing effects, shows  … .

2- Watching is like doing http://www.theglobeandmail.com/technology/science/go-neurons-go-science-explains-why-it-hurts-to-be-a-leafs-fan-sports-diehards-are-wired-that-way/article15214848/

This summer, Australian researchers at the University of Western Sydney published a study in which volunteers lounged comfortably in reclining chairs and watched a bland video of someone walking and running. The faster the person on the screen ran, the higher the pulse and breathing rates of the spectators rose, along with  … .

3. Economy and rate of carbohydrate oxidation during running with rearfoot and forefoot strike patterns.
4. Radiolab.org    
5. Neuromuscular strategies for lumbopelvic control during frontal and sagittal plane movement challenges differ between people with and without low back pain.
6. Achilles: How Much Energy Does Your Achilles Tendon Store? Stiffer tendons help you run more efficiently, but it’s not clear how.
7. Ivo: blog post on toe extensors, the neuromechanics behind it
8. From onlineCE.com, last weeks course
9. Hip centration principles……. principles of accessory motions
from a blog reader
11 Q: can metatarsalgia be caused by ITband tighness ?
 
12. Disclaimer
13. National Shoe Fit program and our Payloadz store
14. Take a monthly course from us at www.OnlineCe.com
 
15. Blog reader:
Guys I feel a little ridiculous asking this ? considering the amount of time I’ve spent reading your info but here goes: I understand the concept of the foot tripod and it’s importance for stabilization and balance when static or during single leg with eg squats, but when should the tripod be utilized during the normal gait cycle?
16 .From a blog reader:
Hello Gentlemen, I was wondering if you could point me in the right direction in terms of addressing a Tailor’s bunion on the 5th met. Thank you!!

Podcast 32: "Shorts"- Stress Fracture Buddies

Today we have a 4 minute short clinical story on a case we saw in the recent weeks. We have searched the medical literature and have not found a study on what we attempted, but we hope that one of our listeners will have found one or had similar experiences and be willing to share their story or a client’s story.

This is a story of a high school middle distance runner who cut her toe, and ended up developing a stress fracture in her metatarsal.  And … . what we attempted to offer immediate change, some theories as to how it worked and how we saved her season (we hope).

Enjoy our short story. 

Imagine, think, ponder, explore and experiment.  Sometimes, you might be surprised what you can come up with, even when it is as simple as something as reaching for a roll of tape.

The Gait Guys

_____________________

podcast link:

http://thegaitguys.libsyn.com/podcast-32-shorts-stress-fracture-buddies

iTunes link:

https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138

Gait Guys online /download store:

http://store.payloadz.com/results/results.aspx?m=80204

other web based Gait Guys lectures:

www.onlinece.com   type in Dr. Waerlop or Dr. Allen  Biomechanics

A case of plantar foot pain during gait.  
 This client came to see us after a surgical proceedure to remove a dead (osteonecrosis) medial sesamoid under the 1st metatarsal head and a later surgery to fix a progressing hammer toe of the 2nd digit. What we really want you to see is the huge divot/depression under the 2-3 metatarsal heads. Also note the accumulation and relocation of the normal MET head fat pad now located distal to the MET heads.  It is as if the fat pad is trying to hitch a ride on the toes now ! This is a case of Metatarsalgia secondary to fat pad displacement (displaced from the divot area to the flexor crease) secondary to surgical sequelae.  
 What is additionally cool in this case is the fact that this client has an almost complete webbing of the 2-3 toes so many of the normal independent muscular functions are no longer independent. After the surgeries this person presents with tremendous loss of flexor and extensor function of the 2-3 toes.  Lumbrical testing was most obviously impaired, completely absent in fact, in these 2-3 toes. On the ground the patient was also unable to achieve any flexion-press of the toes into the ground, he was able to flexion/hammer curl which will obviously put them at risk for hammer toes in the future.  But what is important here is that without the ability to PRESS the toes into the ground particularly while in stance phase the lumbricals will not help to hold the fat pad in its normal location under the MET heads. Nor will they be able to to perform their other major functions, namely:  thinking from a distal to proximal orientation (a closed chain  mode of thinking), they actually plantarflex the metatarsal on the fixed  phalynx, assist in dorsiflexion of the ankle, and help to keep the toes  from clawing from over recruitment of the flexor digitorum longus.   
 This client’s MET head pain is obviously caused by lack of cushioning of the head since the fat pad is displaced. There are plenty of other biomechanical abberancies now, the Windlass mechanism will never be the same becuase it is without one of the sesamoids, the hallux short flexor (FHB) is impaired on the medial head without the sesamoid so hallux flexion will become a problem.  Do we really want to see such compromise of the medial tripod ? Heck no, we need sesamoid implants ! There is a novel idea ! When a sesamoid is taken out we need to replace it ! Think about it ! 
 There is so much more to this case, but we will stop here. It’s Christmas after all ! This poor lady was told to wish from Santa for a medial sesamoid implant under the tree and a sudden spontaneous activation of the lumbricals to retract the fat pad back under the MET head so as to reduce her pain.  Hey, wishing can’t hurt ! 
   Merry Christmas and Happy Holidays to you all gang, whatever your faith we wish you well,   
    from Shawn and Ivo…… The Gait Guys   
 (PS: we included below more from the body of the article we wrote long ago called “The Lost Lumbricals”.  So for those of you who wish to geek out more on Christmas, read on … 
 ______________ 
   EXCERPTS FROM “THE LOST LUMBRICALS”   
 The lumbricals of the foot attach proximally to the sides of adjacent  tendons of the flexor digitorum longus (with the exception of the 1st, which only attaches to the medial side) and attach distally to the medial aspect of the head of the proximal phalynx and continue on to the extensor hoods in toes 2 through 5. Their typical function is described as flexion of the proximal phalynx and extension of the proximal and distal interphalangeal joints. They have the unique ability to compress the metatarsal-phalangeal and interphalangeal joints. These are “open chain” functions as described, unless you are in the habit of waving to people with your toes, they often are used quite differently in the gait cycle with the foot affixed to the ground.  The lumbricals are most active from midstance to preswing. That means they act predominantly in the closed chain. The lumbricals, along with the other intrinsic muscles of the foot, play a role in maintaining the medial longitudinal arch of the foot.  Along with the interossei, they play a role in stabilization of the forefoot during stance phase and rearfoot during preswing. One author has proposed that overpronation is due to a lack of neuromuscular control of the intrinsic foot muscles to stabilize the tarsal and metatarsal bones and therefore modulate the speed of pronation.    Thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.    Clawing toes during gait, which are considered abnormal, are defined as extension of the metatarsophalangeal articulation, and flexion of the proximal and distal interphalangeal joints result from a foot attempting to stabilize itself during the terminal stance and preswing phases of gait.  This is an attempt to help propel the body forward, often accompanied by overactivity of the flexor digitorum longus, tibialis posterior, flexor pollicus longus, and gastroc soleus groups. Overactivity of these groups causes reciprocal inhibition of the long toe extensors and ankle dorsiflexors (tibialis anterior for example), causing the toes to buckle further and a loss of ankle dorsiflexion; in short, diminished ankle rocker.  Now think about the changes in the gait cycle in the above scenario. There will be a resultant shortened step length, diminished ankle rocker, increased forefoot rocker and premature heel rise. This will necessitate an increased extension at the metatarsophalangeal joints, shifting the tendon of the lumbricals upward and behind the transverse metatarsal joint axis, causing even more extension now at this joint.  Chronically over time, this causes displacement of the fat pads anteriorly from under the metatarsal heads and is one of the main reasons metatarsal head pain (metatarsalgia).  In the past have you made the apparent simple diagnoses of metatarsalgia, shin splints, stress fractures or Morton’s neuroma without knowing a more plausible cause ?  Do you now feel you have better answers to these clinical phenomena ?  Now think about changes up the kinetic chain and the potential musculoskeletal implications of muscle inhibition, overfacilitation and joint dysfunction, often with neurological sequelae. With lumbrical dysfunction (weakness) and the resultant lack of ankle dorsiflexion, you have less hip extension.  So, you borrow some from the lumbar spine, with increased compressive forces there and an increase in the lordosis, which causes an increase in the thoracic kyphosis and cervical lordosis. We still need to get this leg up and forward to continue our progression ahead, so now we fire our hip flexors instead of the abdominal obliques. And because there needs to be cooperation of the abdominals and hamstrings to maintain pelvis neutrality, this further fuels inhibition of the gluteals thus further compounding the loss of hip extension. Now how about a little increased shoulder flexion on the contralateral side to assist getting that leg forward? Don’t forget that we have altered the thoracic kyphosis and thus changed scapulo humeral mechanics. Now neck/shoulder pain all from bad feet?  Maybe. These muscles developed and exist for a good reason, do your best not to dismiss them and their function the next time you see a tortured foot.  When patients have continued dysfunction, consider the base and where it all begins. Consider function in the context of where it occurs. Proper evaluation of the feet and gait can provide valuable clues as to the etiology or manifestation of continued problems. Important? You decide.

A case of plantar foot pain during gait.

This client came to see us after a surgical proceedure to remove a dead (osteonecrosis) medial sesamoid under the 1st metatarsal head and a later surgery to fix a progressing hammer toe of the 2nd digit. What we really want you to see is the huge divot/depression under the 2-3 metatarsal heads. Also note the accumulation and relocation of the normal MET head fat pad now located distal to the MET heads.  It is as if the fat pad is trying to hitch a ride on the toes now ! This is a case of Metatarsalgia secondary to fat pad displacement (displaced from the divot area to the flexor crease) secondary to surgical sequelae. 

What is additionally cool in this case is the fact that this client has an almost complete webbing of the 2-3 toes so many of the normal independent muscular functions are no longer independent. After the surgeries this person presents with tremendous loss of flexor and extensor function of the 2-3 toes.  Lumbrical testing was most obviously impaired, completely absent in fact, in these 2-3 toes. On the ground the patient was also unable to achieve any flexion-press of the toes into the ground, he was able to flexion/hammer curl which will obviously put them at risk for hammer toes in the future.  But what is important here is that without the ability to PRESS the toes into the ground particularly while in stance phase the lumbricals will not help to hold the fat pad in its normal location under the MET heads. Nor will they be able to to perform their other major functions, namely: thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

This client’s MET head pain is obviously caused by lack of cushioning of the head since the fat pad is displaced. There are plenty of other biomechanical abberancies now, the Windlass mechanism will never be the same becuase it is without one of the sesamoids, the hallux short flexor (FHB) is impaired on the medial head without the sesamoid so hallux flexion will become a problem.  Do we really want to see such compromise of the medial tripod ? Heck no, we need sesamoid implants ! There is a novel idea ! When a sesamoid is taken out we need to replace it ! Think about it !

There is so much more to this case, but we will stop here. It’s Christmas after all ! This poor lady was told to wish from Santa for a medial sesamoid implant under the tree and a sudden spontaneous activation of the lumbricals to retract the fat pad back under the MET head so as to reduce her pain.  Hey, wishing can’t hurt !

Merry Christmas and Happy Holidays to you all gang, whatever your faith we wish you well,

from Shawn and Ivo…… The Gait Guys

(PS: we included below more from the body of the article we wrote long ago called “The Lost Lumbricals”.  So for those of you who wish to geek out more on Christmas, read on …

______________

EXCERPTS FROM “THE LOST LUMBRICALS”

The lumbricals of the foot attach proximally to the sides of adjacent  tendons of the flexor digitorum longus (with the exception of the 1st, which only attaches to the medial side) and attach distally to the medial aspect of the head of the proximal phalynx and continue on to the extensor hoods in toes 2 through 5. Their typical function is described as flexion of the proximal phalynx and extension of the proximal and distal interphalangeal joints. They have the unique ability to compress the metatarsal-phalangeal and interphalangeal joints. These are “open chain” functions as described, unless you are in the habit of waving to people with your toes, they often are used quite differently in the gait cycle with the foot affixed to the ground.

The lumbricals are most active from midstance to preswing. That means they act predominantly in the closed chain. The lumbricals, along with the other intrinsic muscles of the foot, play a role in maintaining the medial longitudinal arch of the foot.  Along with the interossei, they play a role in stabilization of the forefoot during stance phase and rearfoot during preswing. One author has proposed that overpronation is due to a lack of neuromuscular control of the intrinsic foot muscles to stabilize the tarsal and metatarsal bones and therefore modulate the speed of pronation.

Thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

Clawing toes during gait, which are considered abnormal, are defined as extension of the metatarsophalangeal articulation, and flexion of the proximal and distal interphalangeal joints result from a foot attempting to stabilize itself during the terminal stance and preswing phases of gait.  This is an attempt to help propel the body forward, often accompanied by overactivity of the flexor digitorum longus, tibialis posterior, flexor pollicus longus, and gastroc soleus groups. Overactivity of these groups causes reciprocal inhibition of the long toe extensors and ankle dorsiflexors (tibialis anterior for example), causing the toes to buckle further and a loss of ankle dorsiflexion; in short, diminished ankle rocker.

Now think about the changes in the gait cycle in the above scenario. There will be a resultant shortened step length, diminished ankle rocker, increased forefoot rocker and premature heel rise. This will necessitate an increased extension at the metatarsophalangeal joints, shifting the tendon of the lumbricals upward and behind the transverse metatarsal joint axis, causing even more extension now at this joint. Chronically over time, this causes displacement of the fat pads anteriorly from under the metatarsal heads and is one of the main reasons metatarsal head pain (metatarsalgia). In the past have you made the apparent simple diagnoses of metatarsalgia, shin splints, stress fractures or Morton’s neuroma without knowing a more plausible cause ?  Do you now feel you have better answers to these clinical phenomena ?

Now think about changes up the kinetic chain and the potential musculoskeletal implications of muscle inhibition, overfacilitation and joint dysfunction, often with neurological sequelae. With lumbrical dysfunction (weakness) and the resultant lack of ankle dorsiflexion, you have less hip extension.  So, you borrow some from the lumbar spine, with increased compressive forces there and an increase in the lordosis, which causes an increase in the thoracic kyphosis and cervical lordosis. We still need to get this leg up and forward to continue our progression ahead, so now we fire our hip flexors instead of the abdominal obliques. And because there needs to be cooperation of the abdominals and hamstrings to maintain pelvis neutrality, this further fuels inhibition of the gluteals thus further compounding the loss of hip extension. Now how about a little increased shoulder flexion on the contralateral side to assist getting that leg forward? Don’t forget that we have altered the thoracic kyphosis and thus changed scapulo humeral mechanics. Now neck/shoulder pain all from bad feet?  Maybe. These muscles developed and exist for a good reason, do your best not to dismiss them and their function the next time you see a tortured foot.

When patients have continued dysfunction, consider the base and where it all begins. Consider function in the context of where it occurs. Proper evaluation of the feet and gait can provide valuable clues as to the etiology or manifestation of continued problems. Important? You decide.