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

IMG_1603.jpg

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

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


Could your low back pain be related to your big toe?

Ok, he has low back pain. But i can also see that high gear (1st toe off) is impaired from loss of terminal dorisflexion at that 1st MTP joint.

Ok , so this means heel rise will be premature and when it does happen the toe off will be towards the lesser toes, low gear toe off.
This means the knee will be carried laterally as opposed to the more desirable sagittal tracking/hinging.
And, if heel rise is premature, this means the knee will likely flex and hinge sagittally just a little, when it should actually be extending and coupling with the gastroc and glute to produce propulsion.
And, when the knee flexes, I know the hip flexes, when we should again be moving into hip extension for propulsion.
And when the knee and hip flex, the vertical length of the leg is shorter functionally, which means a subtle lateral pelvis dip and compensatory thoracolumbar lateral bend to the other side to compensate. This leads to imbalance in the lumbar spine musculature and more work in some areas, and less in others.

So, doc, are you telling me my low back pain is from my big toe? It could be Sir. Lets get into it and find out.
Game ?
Game . . . .

One has to be able to quickly juggle normal known gait biomechanics with pathologic biomechanics. You don't have all day with your patient. Play these games in your head, often.
Example: So, if the knee doesn't terminally extend, what could this mean to the rest of the system ?

Stop treating the area of pain, is might not be the problem.

Shawn Allen, one of the gait guys.

#gait, #thegaitguys, #gaitproblems, #gaitcompensations, #halluxlimitus, #turftoe, #hipextension, #prematureheelrise

Do you really understand what it takes to control the 1st Metatarsal during loading ?

Do you have dorsal (top) foot pain, at the peak of the arch? Think you are tying your shoes too tightly and that is the cause? Do you have pain over the dorsal or plantar mid foot on heel rise or jumping/landing or going up stairs ?

Just because you raise your heel and load the ball of the foot does not necessarily mean you have adequately plantarflexed the 1st metatarsal and loaded it soundly/stable with the medial tarsal bone. Heel rise, and thus loading onto the medial foot tripod, must be met with ample, stable, durable, 1st metatarsal plantarflexion and the associated medial tarsal bones. Also, without this, loading of the sesamoids properly cannot occur, and pain may ensue.

The first ray complex can be delicate in people who are symptomatic. In some people who do not have a good tibialis posterior-peroneus sling mechanism working harmoniously, in conjunction with a competent arch tripod complex to achieve a compentent arch complex (ie, EDL, EHL, tib anterior and some of the other foot intrinsics) this tarsometatarsal interval can become painful and instead of the 1st ray complex being stable and plantarflexing as the heel departs and the 1st ray begins taking load, it may not do so in a stable plantarflexed posturing. In some people it can momentarily dorsiflex as the arch subtly collapses (when it should be stable and supinated in heel rise).

"Subtle hypermobility of the first tarsometatarsal joint can occur concomitantly with other pathologies and may be difficult to diagnose. Peroneus Longus muscle might influence stability of this joint. Collapse of the medial longitudinal arch is common in flatfoot deformity and the muscle might also play a role in correcting Meary's angle."-Duallert et al

Soon, I hope to show you a video of how to watch for this problem, how to train it properly, how we do it in my office.
Dr. Allen

Reference:

Clin Biomech (Bristol, Avon). 2016 May;34:7-11. doi: 10.1016/j.clinbiomech.2016.03.001. Epub 2016 Mar 10.  The influence of the Peroneus Longus muscle on the foot under axial loading: A CT evaluated dynamic cadaveric model study. Dullaert K1, Hagen J2, Klos K3, Gueorguiev B4, Lenz M5, Richards RG6, Simons P7.

https://www.ncbi.nlm.nih.gov/pubmed/27015031

Plantar flexion matters, too. Don't get stuck only on ankle rocker/dorsiflexion.

Screen Shot 2018-02-03 at 11.54.39 AM.png

Plantarflexion matters, too.
"one must gain posterior length through anterior strength, lose the strength, lose the length."

We always seem to be harping on ankle rocker and ankle dorsiflexion. But, ankle plantarflexion matters just as much, but in different ways. This study went off of plantarflexion contracture, but we see shortness in the gastroc and soleus all the time, it seems in fact to go with loss of anterior compartment weakness, which is in essence, a functional (if not more truly restricted) loss of ankle rocker. Typically these 2 beasts are both in the same shopping bag. It is why we like to say, "one must gain posterior length through anterior strength, lose the strength, lose the length." This is not to say that shortness, tightness or contracture are the same thing, in fact they are on completely different spectrums. But, losing "posterior mechanism" length (short, tight or contracture), for whatever reason will do many potentially bad things to one's gait cycle and biomechanics. There are too many here of those to name, but, a functionally longer leg, tendency towards knee extension, knee flexion accomodation, early heel rise, abrupt departure from the limb and and abruptly onto the contralateral side, increased forefoot loading problems, toe clenching, loss of hip extension, impaired hip extension, increased quadriceps tone (and thus possible increased PF joint compression), changes in step and stride length and step width are just the start of some of the things your brain needs to start juggling.

The above are some of the thoughts immediately triggered by reading this abstract , , ,

Clinical Biomechanics. Volume 29, Issue 4, April 2014, Pages 423-428
The impact of simulated ankle plantarflexion contracture on the knee joint during stance phase of gait: A within-subject study
Joan Leung, Richard Smith, Lisa Anne Harvey. Anne M. Moseley, JosephChapparo

A fresh calf tear. Video case

As fresh as fresh gets, trauma hours ago. Running in soft sand, felt a pop left medial calf.
So, is it:
1. a full medial head tear ?
2. Partial low grade tear that has just bled into the area that normally would have shown the medial calf definition? ie Bleeding blurring the definition ?
3. Muscular pain inhibition because the calf raise is painful ?
The latter two of the 3 ?
All the above?
Saving grace, there is a palpable medial calf contraction, it is just not authoritative like the other leg, painful to engage.
So, MRI ? If not even considering surgery regardless, does it change our treatment ? Let it heal and deal with the aftermath ?
Wait and see ? If in a few days-week the swelling and pain inhibition reduce and the strength comes back, regardless of definition restoration, is that a bullet dodged ?
What would you do ?

* injury is on the left, i am pointing to the normal defniition on the right. Note the absense on the left.

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

This is apparently a growing thing, INTERVAL walking. Oy. We are not particular fans at this point, nothing exciting or earth shattering at this point (other than the concerns we hi light below) but we will look into it more.
What you need to see, and be aware of, is that this is what happens when you wear a shoe that has too soft a rear foot. At heel strike, instead of progressing forward into the mid and forefoot, the rear foot of the shoe deforms and forces you into more HEEL rocker, sustained heel rocker. If you stay in heel rocker too long, you won’t progress forward into ANKLE rocker (ankle dorsiflexion). This often causes knee hyperextension. If you have a good trained eye, you will see both of these things, prolonged heel rocker and never any ankle rocker/ankle dorsiflexion. IT is like the ankle in this video is frozen at 90 degrees the entire time, train your eye to see this absense of ankle rocker. This will cause premature heel rise and premature posterior compartment contraction which can cause premature forefoot loading. This is what happens when the heel of the shoe is too soft. A perfect example of “more cushion” is not always better. IT can be a liability as well. Remember the angry revolution over the MBT shoe and its mushy rear foot?. Same principle, same risks and concerns. Welcome to round two of the same old problems ????? Maybe. you decide. To be clear, this is a comment on the shoes being used, the technique is , well, perhaps interesting. That is all we are willing to comment on at this point until we look into it more. Look at the heel and ankle mechanics during the slow mo clips.
Sorry Ben Greenfield. We are not impressed, as of yet. We like your podcast Ben, you are doing us all a great service, but this one is promoting some potential problems that people need to know about.
Start with our “Shuffle Walk”. Google search it under the Gait Guys. That is a good start.

- Dr. Allen

The Abductor Heel Twist: Look carefully, it is here in this video.

This should be a simple “piece it together” video case study for you all by this point. This young lad came into our office with left insertional achilles pain of two weeks duration after starting some middle distance running.

What do you see here ? It is evident on both the right and the left, but it is a little more obvious on the left and can be seen on the left when he is walking back toward the camera as well.  You should see rearfoot eversion, it is excessive, and a small rearfoot adductor twist. Meaning, the heel pivots medially towards the midline of his body.  Some sources (Michaud) call this an Abductory Twist, but the reference there is typically the forefoot.  Regardless, to help our patients, we sometimes refer to this is “cigarette butt” foot. It is like stepping on a lit cigarette to put it out via twisting/grinding it into the ground. 

So, now that you can see this, what causes it? 

The answer is broad but in this case he had a loss of ankle dorsiflexion range.  The ankle mortise clearly did not have enough of ankle rocker range during midstance so as that limitation was met, the heel raised up prematurely during the moments when the opposite leg is in full swing imparting an external rotation on the stance limb (hence the external foot spin (adducting heel/abducting foot……depending on your visual reference)). There is a bit more to it than that, but that will suffice for now because it is not the central focus of our lesson today.

What can cause this ? As we said, a broad range of things:

  • hallux limitus
  • flexion contracture of the knee (swelling, pain, joint replacement etc)
  • short calf-achilles complex
  • weak tib anterior and extensor toe muscles
  • Foot Baller’s ankle
  • limited/impaired hip extension
  • weak glute (minimizing hip extension range)
  • sway back (lower crossed syndrome-type biomechanics)
  • short quadriceps (similarly impairing hip extension)
  • flip flop excessive use (or any other motor strategy that imparts more flexor compartment dominance (read: calf-achilles, FDL)
  • excessive pronation
  • impaired foot tripod mechanics
  • etc

The point is that anything impairing TIMELY (the key word is timely) forward sagittal gait mechanics can, and very likely will, impair ankle rocker.  Even the wrong shoe choice can do this (ie. someone who suddenly drops from a 12 mm heel ramped shoe into a 0-4mm ramped heel shoe and who thus may not have earned the length of the calf-achilles complex as of yet).

The abductor-adductor twist phenomenon is not a normal visual gait observation. It is a softly seen, but screaming loud, pathologic gait motor pattern that must be recognized.  But, more importantly, the source of the problem must be found, confirmed and resolved.  In this fella’s case, he has some weakness of the tib anterior and extensor toe muscles that has lead to compensatory tightness of the calf complex. There was no impairment of the glutes or hip extension, as this was just 2 weeks old or so, but if left unaddressed much longer the CNS would have likely begun to dump out of hip extension and gluteal function to protect……another compensation pattern. Remember, ankle rocker and hip extension have a close eye on each other during gait.

Clinical pearl for the true gait geeks…… if you see someone with a vertically bouncy forefoot-type gait (you know, those people that bounce up and down the hallway at work or school) you can usually suspect impaired ankle rocker and if you look closely, you will usually see a quick abductor-adductor twist.

Shawn and Ivo

the gait guys

The weeping calf and the deconstructed arm swing.

Last week we showed you this video and blog post of a compressive left lower leg neuropathy and what it looks like when both heel and toe walking are attempted when both are compromised. It was nothing exciting but to see both in a clinical presentation is not all that common.

In today’s videos (the one above and this one here), the videos were all shot on the same day incidentally, we wanted you to see this gentleman’s gait in it’s normal gait pattern attempt.  Because less of the extremes of range and strength are required, it is far more difficult to detect the issues than in last week’s video clip (here).

There are plenty of things to talk about in this video but lets just point out one of them here today.  Remember, the lesion is in the left lower leg.

Absent right arm swing. 

We have been harping about arm swing for a long time.  Go to the search box here on our blog and type in “arm swing” and you will find an abundance of articles on the biomechanics and neurology of arm swing and how it is tied to leg swing.  In this case we have foot drop and impaired calf raise (video link) on the left. Their function is impaired/depressed. We are seeing this matching in the absence of right upper limb swing.  Remember, most of the time the upper limb takes the queue from the opposite lower limb. This is why coaching arm swing changes is not a sound idea most of the time, look for functional opportunities for changes in the opposite lower limb if deficits are present there.  

Part of what you are seeing is the increased activity in the left arm swing.  Why ? Because the client is abruptly lurching off of the left leg because of the stability and strength deficits in that limb. The brain knows that bearing weight on the left limb has challenges.  This causes an abrupt pitch (early departure) forward onto the right leg and this will be met with increased left arm swing (go limb around your home or office, you will see that it is a coupled phenomenon).  So, is it increased left arm swing you are seeing because of this issue we just mentioned or are you seeing decreased right arm swing because of the matching neuro-suppression of left leg ? 

This is where your clinical examination must come into play. Shame on anyone that is making the changes without clinical information. One must see that there rare two (at least) possible scenarios for the differential in arm swing. And one must also see that the arms in this case are not the issue, that it is the left lower limb deficits that are driving the issue.  Guaranteed.

Arm swing……..more to it than you might think.

Shawn and Ivo, The gait guys

A Serious Gait Problem: Pancompartmental Compromise of the Lower Leg.

“Pan” is a prefix (combining form) meaning all, entire, everything, everywhere 

This was a case we discussed during a more recent podcast, perhaps pod 63 or 64? This doctor had fallen asleep with the left leg dangling over the side of his bed. The issue was that the leg not only dangled over the mattress, but also over a wooded side bed frame, so there was a firm upward compression into the posterior/popliteal compartment. He awoke the next day with complete loss of function of the foot and ankle.  This video is 8 weeks after the compressive event and there has been a significant improvement in function, but there are still some deficits here.  Can you see them ?  We will show you come other video clips in a future blog post discussing some other components of his gait but lets get you familiar with the case today.

What you should see here:

1- Left heel shows a staggered drop. He cannot hold heel rise because of compromise to the posterior compartment strength (gastrocsoleus complex). This was a drastic improvement from his complete inability to heel rise at all at on his initial visit. You can easily see the fatiguability of the calf after just a few steps. 

2- There is a pathetic attempt at heel walking; gross function testing of the anterior compartment. What appears to be an attempt at just right heel walking is actually an attempt to do it on both sides, there is just still so much weakness in the left anterior compartment that you cannot even see his attempts to dorsiflex the foot/ankle or toes. But, what we do not show here is that he has non-weight bearing dorsiflexion now, which was completely absent for the first 6 weeks.  

Neuronal regeneration is possible. It takes time.  Depending on your referenced source the numbers vary. But in his case, in 8 weeks there is progressive improvements and he can say for certain that in the last 2 weeks they are exponential.  The time to restoration of neuronal function is said to be directly proportional to the measurable length of nerve damage.  

What is interesting in this case, is that there is anterior and posterior compartment neurologic compromise. This was a case of vascular and mechanical compression to the neurovascular bundle at the popliteal/knee level. 

Wallerian degeneration is a process that results when a nerve is severely damaged. The axon of the nerve which is separated from the neuron cell body degenerates distal to the injury. The part of the axon distal to the injury begins its degeneration within 24-36 hours of the lesioning event and is followed by myelin sheath degradation. Somewhere around 4 days from the time of the injury, the distal end of the portion of the nerve fiber proximal to the lesion begins sprouting in an attempt to regrow and fill the gap along the length of axonal damage. Sources vary, but many seem to indicate a 1mm per day reinnervation. 

More on this case next time, but the stage has been set.

Shawn and Ivo

More Foot Rocker pathology Clues. 
 Is ankle rocker normal and adequate or is it limited ?  Is it limited in early midstance or late midstance ? How about at Toe off?  Is it even possible to distinguish this ? Well, we are splitting hairs now but we do think that it is possible. It is important to understand the pathologies on either end of the foot that can impact premature ankle rocker.  
 Look at the photo above. You can see the clinical hint in the toe wear that this runner may have a premature heel rise. However, this is not solid evidence that every time you see this you must assume pathologic ankle rocker. The question is obviously, what is the cause. 
 Considerations: 
 1- weak anterior compartment, which is quite often paired with the evil neuroprotective tight calf-achilles posterior complex to offer the necessary sagittal protection at the ankle mortise.  This will cause premature heel rise from a posterior foot aspect. 
 2- rigid acquired blocked ankle rocker from something like “Footballer’s ankle”.  This will also cause premature heel rise from a relatively posterior foot aspect.  
  3- there are multiple reasons for late midstance ankle rocker pathology. The client could completely avoid the normal pronation/supination phase of gait because of pain anywhere in the foot. For example, they could have plantar fascial pain, sesamoiditis, a weak first ray complex from hallux vaglus, they could have a painful bunion, they could be avoiding the collapse of a forefoot varus. There are many reasons but any of them can impair the timely pronation-supination phase in attempting to gain a rigid lever foot to toe off the big toe-medial column in “high gear” fashion. And when this happens the preparatory late midstance phase of gait can be delayed or rushed causing them to move into premature heel rise for any one of several reasons.  Rolling off to the outside and off of the lesser toes creates premature heel rise.    
  4- And now for one anterior aspect cause of premature heel rise. This is obviously past the midstance phase but it can also cause premature heel rise. Turf toe, Hallux rigidus/limitus or even the dreaded fake out, the often mysterious Functional Hallux limitus (FnHL) can cause the heel to come up just a little early if the client cannot get to the full big toe dorsiflexion range.    
 We could go on and on and include other issues such as altered Hip Extension Patterning, loss of hip extension range of motion, weak glutes, or even loss of terminal knee extension (from things like an incompleted ACL rehab, Osteoarthritis etc) but these are things for another time. Lets stay in the foot today. 
 All of these causes, with their premature heel rise component, will rush the foot to the forefoot and likely create Metatarsal head plantar loading and could cause forces appropriate enough to create stress responses to the bone. This abrupt forefoot loading thrust will often cause a reactive hammer toe effect.  Quite often just looking at the resting nature of a clients toes while they are lying down will show the underlying increase in neuro-protective hammering pattern (increased long toe flexor and short toe extensor activity paired with shortness of the opposing pairs which we review here in  this short video link ).  The astute observer will also note the EVA foam compressing of the shoe’s foot bed, and will also note the distal displacement of the MET head fat pad rendering the MET head pressures even greater osseously.  
 Premature ankle rocker and heel rise can occur for many reasons. It can occur from problems with the shoe, posterior foot, anterior foot, toe off, ankle mortise, knee, hip or even arm swing pathomechanics.   
 When premature heel rise and impaired ankle rocker rushes us to the front of the foot we drive the front half of the shoe into the ground as the foot plantarflexion is imparted into the shoe.  The timing of the normal biomechanical events is off and the pressures are altered.  instead of rolling over the forefoot and front half of the shoe after our body has moved past the foot these forces are occurring more so as our body mass is still over the foot. And the shoe can show us clues as to the torture it has sustained, just like in this photo case. 
 You must know the normal biomechanical gait events if you are going to put together the clues of each runner’s clinical mystery.  If you do not know normal how will you know abnormal when you see it ? If all you know is what you know, how will you know when you see something you don’t know ? 
 Shawn and Ivo, The Gait Guys … .  stomping out the world’s pathologic gait mechanics one person at a time. 

More Foot Rocker pathology Clues.

Is ankle rocker normal and adequate or is it limited ?  Is it limited in early midstance or late midstance ? How about at Toe off?  Is it even possible to distinguish this ? Well, we are splitting hairs now but we do think that it is possible. It is important to understand the pathologies on either end of the foot that can impact premature ankle rocker. 

Look at the photo above. You can see the clinical hint in the toe wear that this runner may have a premature heel rise. However, this is not solid evidence that every time you see this you must assume pathologic ankle rocker. The question is obviously, what is the cause.

Considerations:

1- weak anterior compartment, which is quite often paired with the evil neuroprotective tight calf-achilles posterior complex to offer the necessary sagittal protection at the ankle mortise.  This will cause premature heel rise from a posterior foot aspect.

2- rigid acquired blocked ankle rocker from something like “Footballer’s ankle”. This will also cause premature heel rise from a relatively posterior foot aspect.

3- there are multiple reasons for late midstance ankle rocker pathology. The client could completely avoid the normal pronation/supination phase of gait because of pain anywhere in the foot. For example, they could have plantar fascial pain, sesamoiditis, a weak first ray complex from hallux vaglus, they could have a painful bunion, they could be avoiding the collapse of a forefoot varus. There are many reasons but any of them can impair the timely pronation-supination phase in attempting to gain a rigid lever foot to toe off the big toe-medial column in “high gear” fashion. And when this happens the preparatory late midstance phase of gait can be delayed or rushed causing them to move into premature heel rise for any one of several reasons.  Rolling off to the outside and off of the lesser toes creates premature heel rise.  

4- And now for one anterior aspect cause of premature heel rise. This is obviously past the midstance phase but it can also cause premature heel rise. Turf toe, Hallux rigidus/limitus or even the dreaded fake out, the often mysterious Functional Hallux limitus (FnHL) can cause the heel to come up just a little early if the client cannot get to the full big toe dorsiflexion range.  

We could go on and on and include other issues such as altered Hip Extension Patterning, loss of hip extension range of motion, weak glutes, or even loss of terminal knee extension (from things like an incompleted ACL rehab, Osteoarthritis etc) but these are things for another time. Lets stay in the foot today.

All of these causes, with their premature heel rise component, will rush the foot to the forefoot and likely create Metatarsal head plantar loading and could cause forces appropriate enough to create stress responses to the bone. This abrupt forefoot loading thrust will often cause a reactive hammer toe effect.  Quite often just looking at the resting nature of a clients toes while they are lying down will show the underlying increase in neuro-protective hammering pattern (increased long toe flexor and short toe extensor activity paired with shortness of the opposing pairs which we review here in this short video link).  The astute observer will also note the EVA foam compressing of the shoe’s foot bed, and will also note the distal displacement of the MET head fat pad rendering the MET head pressures even greater osseously. 

Premature ankle rocker and heel rise can occur for many reasons. It can occur from problems with the shoe, posterior foot, anterior foot, toe off, ankle mortise, knee, hip or even arm swing pathomechanics.  

When premature heel rise and impaired ankle rocker rushes us to the front of the foot we drive the front half of the shoe into the ground as the foot plantarflexion is imparted into the shoe.  The timing of the normal biomechanical events is off and the pressures are altered.  instead of rolling over the forefoot and front half of the shoe after our body has moved past the foot these forces are occurring more so as our body mass is still over the foot. And the shoe can show us clues as to the torture it has sustained, just like in this photo case.

You must know the normal biomechanical gait events if you are going to put together the clues of each runner’s clinical mystery.  If you do not know normal how will you know abnormal when you see it ? If all you know is what you know, how will you know when you see something you don’t know ?

Shawn and Ivo, The Gait Guys … .  stomping out the world’s pathologic gait mechanics one person at a time. 

Pathologic Ankle Rocker: Part 2. “Passing the Buck Proximally”

This was an unexpected follow up blog post from yesterday’s piece we did on the rigid flat foot. We were purging some files from an old computer and came across these 2 videos. We are not even sure where they came from. They were AVI files from probably 2 decades gone by;  they reminded us how long we have been at this gait game and how many great patients have taught us along the way.
Yesterday we learned that if the ankle rocker (dorsiflexion) was impaired that we could ask for the motion to be passed into the midfoot via hyperpronation in order to get the tibia to progress past vertical to enable the body to pass by the rigid ankle mortise rocker.  (Remember from our previous teachings that there are 3 rockers in the foot. First there is heel rocker, then ankle rocker, then forefoot rocker. Each is essential for normal gait. You must understand the 3 rockers to understand gait and to recognize gait pathologies when they present.)
So, yesterday we saw a strategy of pronating excessively through the midfoot to artificially trick us into thinking we have more ankle rocker then we actually truly did. So this was a “pass the buck” into the foot. Today however we are going to show you a very atypical compensatory choice. Today this client shows that with a rigid and/or strong enough arch that the arch doesn’t always need to be the part that gives in to enable more rocker. Today this client chose a vertical strategy.
You are going to have to study these videos closely several times, this is a critical learning and teaching point today. The problem is the left ankle in the video.

This client has chosen to go  VERTICAL when they hit the ankle rocker limitation. Once they achieve their terminal range at the ankle mortise joint (the tibio-talar joint ) their brain realized that moving forward at the ankle was impossible. Since the midfoot did not collapse and give in, as in yesterday’s case, they had no choice but to “pass the buck” proximally into the kinetic chain. In this case we see that the knee was the next vertical joint. Now, they have 2 choices, either hyperextend the knee to enable a forward lurch of the body mass past the ankle rocker axis or “go vertical”. In this case you can see the early heel rise (we refer to is as premature heel rise). Frequently a premature heel rise can force knee flexion but in this case the rise just kept going vertical and forcing them into the use of the gastrocsoleus group and thus forcing a lift of the entire body. If you look hard you can see a greater development of the calf muscles on this side from doing this for years. (Oh, wait, memory data dump here…..we are recalling this case, it was the result of an old motorcycle accident. A student sent us this video back in the 1990’s when we were teaching at the university.)
What is interesting here is that if you think hard, and this will be a new thought process for many readers, that when he goes into heel rise he buys himself more ankle range again. You see, he first met the end range limitation of ankle rocker which appears to be about 90 degrees and then he hits the bony block. If he goes vertical into the calf he is moving back into plantarflexion. This means that even though he is on the forefoot now, he has bought himself more ankle dorsiflexion range again. Now he has the option of holding the posture on the forefoot as rigid and then re-utilizing the new-found extra degrees of ankle dorsiflexion to progress forward OR, he can just move into FOREFOOT ROCKER (the 3rd of the rockers we meantioned earlier).  This client is likely doing a bit of both, perhaps a little more of the forefoot rocker strategy.
You can also kind of see that this slightly shortens the time in the stance phase on this left side and causes an early dumping onto the right limb (which causes a frontal plane pelvis distortion compensation). This gives the appearance of a slight limp.
So, this was a nice follow up from yesterday’s principle of “passing the buck”. You can either ask for the motion from the next distal joint in the kinetic chain, or  you can back up the kinetic chain and dump it into the proximal joint from the pathologic one (the knee in this case). Which one would you want, if you had to choose?  It is a tough choice, luckily the body decides for us.  IF you consider that luck !

Regardless, one has to stand in awe that the body will find a way to get the range elsewhere when it cannot find it in the primary motor pattern.  And when the range has to be gained elsewhere, the muscular function has to change as well and prostitute the normal kinetic chain motor patterns.

Here is a tougher question for you. Would you want this phenomenon on one side and be unilaterally compromising (and thus have to compensate on the opposite side) the kinetic chain or bilaterally and have the asymmetry on both sides ?  That is a tough one. There is no good choice however.

*Please do not try to help this client by putting a heel wedge in their shoe. You are just going to rush heel rocker into that bony block sooner and faster and speed up his pathologic stance phase. You will see his vertical strategy come even faster and thus pass the buck into the opposite right hip even stronger. It is a fleeting good initial thought because you are merely trying to help his poor calf muscles get to that heel rise easier, until you think about it for a minute.

When it comes to the feet, use your head.  And, consider the Gait Guys, National Shoe Fit DVD program.  Email us at : thegaitguys@gmail.com

Yesterday’s Video Case: The Gaits of Hell

We have received many emails on this case already. Overwhelmingly people are saying……. “Hey, this isn’t easy….. It’s easy when you guys tell us right away because we can see it."  
Yes, when we are all alone to solve these gait problems our heads can start to swim with all the variables. Gait analysis is not easy.  Even the video assessment computer programs do not give you the answers and diagnosis, they just give you variables and data.  The thinking still has to be  done at the end of the day.


I remember how much I struggled with this case back during my orthopedics residency. I remember even pulling out my undergrad notes from Univ. of Waterloo as a student of the famous Dr Stewart McGill and mapping out FBD’s (Force-Body Diagrams) on this case. Oh, the horror !!!  I still have occasional FBD nightmares, being asked to solve an equation in front of the whole class. Pure anxiety ! Holy night terrors ! But, it is amazing what a few decades of study will do for you, we can now look at this case and see things for what they are, see them quickly and know what is going on almost immediately.  It takes some time, so if you are new to this stuff, be patient…… it will come.

CASE REVIEW:

in this video we see the following:

  1. large step length off of the left foot abruptly onto the right, this step is sudden and he crashes down on to the right foot sooner than he normally would to catch his forward moving body mass. ( this will make more sense after reading #5).
  2. there is a delayed left heel rise and delayed left calf recruitment , actually, it’s not delayed, it’s absent. )
  3. the left foot remains supinated through the entire gait cycle. 
  4. the left foot shows extraordinary long toe flexor recruitment (seen on the end of the video during the foot close up)…….this point is important
  5. pelvic unleveling is apparent but a mirage for the most part. We really do not see a true Trendelenberg style gait (although it sort of looks like the left hip drops) rather, what you see is the result of the manufactured delayed left limb departure and subsequent impact at right limb load … but this is not a Trendelenberg gait, he had no Gluteus medius weakness.  Explained another way, he is having troubles departing off of the left foot (this diagnosis is the reason, he has compensated from a neurologic lesion affecting the strength of the calf) and so he extends ( behind him) the left leg longer and further than normal because he cannot push off, plus he hyperextends the left knee because of these factors. Normally, the calf fires after passive heel lift occurs. But with a lesion affecting the calf it has arrested the push off. So, in his case, the heel stays on the ground until it is dragged off from enough  forward body carriage. So, when you see this from a sagittal view the left hip will look like it is dipping as it does here, but it is not truly, he is just taking a long lurching step off of the left and onto the right, the longer left hip extension behind him sets up the illusion of a left hip drop.  Try this at home to feel this gait, walk down your hallway and try to delay the left heel rise for as long as you can.  You will find that you get into your left gluteals more, take a longer step on the left, and take a sudden lurching load onto the right limb to catch your forward progressing body mass. This is exactly what this chap is doing.  But why ? The left calf lesion. 
  6. continuing on #5, there is abrupt right frontal plane loading (because of the sudden transition from left foot to right the frontal plane is engaged longer than normal) and thus the pelvis is carried further to the right in the frontal plane.  He makes a  noble attempt to protect this range by turning out the right foot into the frontal plane (aka. increased right foot progression angle) to allow the quadricep muscles to assist the gluteus medius, abdominal obliques and lateral limb stabiliers in decelerating this frontal plane challenge.

Diagnosis:This doctor came to see me while I was completing my orthopedics residency and mid way through my course work in the neurology post doctoral program. He had been treated for mechanical low back pain with failed results ( well, to be accurate. his low back pain had resolved but pain had peripheralized into the left leg. To review, peripheralizing pain is rarely a good neurologic sign.)  After an examination showing an absent left S1 Achilles reflex it was highly suspicious we were dealing with a radiculopathy. An MRI confirmed a substantial left foraminal disc herniation obliterating the left S1 nerve root foraminally. The S1 nerve root expands into branches feeding input into the lower limb muscles.  In this case, the unfortunate group affected was the gastrocnemius almost exclusively. So in this case this makes sense to what is presented clinically and on gait evaluation. He is overutilizing his long toe flexors (fortunately untouched) as seen in the video because they are basically all that is available to him to plantarflex the foot ( create heel rise and push off).  They are certainly not well suited for this task but subconsciously the brain will use what is available to it, worthy or not. In this case they are a feeble attempt at best. There is no way the long toe flexors can lift his body mass into heel rise and propulse it forward, they are synergists of this task and not agonists / prime movers.
Sequencing Summary:So, this is a case of an aberrant or pathological gait pattern that will be permanent because the nerve damage was fixed by the time i had seen him.  Muscular wasting of the gastroc complex had already occurred.  The culprit was the space occupying lesion (disc in this case) in the left spinal vertebral foramina effacing and deforming the nerve root sufficient enough to create dennervation.  A surgical consult and EMG/NCV (as best as i can recall) confirmed this case was non-surgical at that time (no one wanted to touch the case).  The nerve damage disabled the calf so that push off was impaired.  He thus delays his ability to create adequate heel rise and propulsion so the long toe flexors are called to attempt the feat.  The foot supinates to maintain its rigidity ( it is also hard to pronate through the foot when the toe flexors are in an all out contraction). And because the heel does not rise on its own from muscular strategies, the foot waits to be lifted off of the ground by simple forward progression of the body.  This creates an increased left hip extension range and gives the appearance of a left hip drop which is a false appearance pseudo-Trendelenberg sign.  Due to the fact that he is on the left limb longer, he will be on the right limb for a shorter period.  This right stance phase is initiated abruptly as he falls from the delayed left stance phase. The abruptness of the load on the right challenges the right frontal plane as evidenced by the right foot turn out and right pelvis sway (subtle).  He then departs off the right to  begin the cycle once again.
PS: It is coming a little late, but thank you Dr McGill. Your teachings to a young undergrad set my biomechanical thinking on the right path very early in my studies of human kinetics. Thank you, Sincerely. 
Dr Shawn Allen…… The other half of The Gait Guys

iWalk Powerfoot video Army

Here in this video our keen eye was correct regarding the reduction in ankle rocker and subsequent heel rise.  The video when the soldier is walking down the stairs (most notable for on the last step) gives an excellent example of what happens when ankle rocker (tibiotalar dorsiflexion) is impaired (this can look like another clinical condition called FootBaller’s ankle if a spur develops). See how much knee lift he has to generate, forced by the early heel rise.  Once again, still an amazing piece of engineering.

(* If the fabricators are reading this, we are here to help !  Start by moving that metal bar at the front of the “mortise” another few millimeters forward and you will get the extra few degrees to reduce that rocker/heel lift issue. This will smooth out mechanics at the hip and knee and add to user stability and balance.)

iWalk PowerFoot Gait Animation

Check out this 3 million dollar bionic foot! For a walking gait cycle (not running cycle) it shows excellent heel rocker; and the appearance of a little hallux limitus (an articulating first metatarsophalangeal joint with an eccentric axis is likely a bit complicated to produce)…….But, for all that money you would have thought they could have added more ankle rocker ! The model gets to what looks like about 110-115 degrees which is the lower limit of what is necessary. It is why you see such an early heel rise in the video.  Why don’t folks just call us…..we would have  taken $100,000 for a consulting fee on this one to help them get it right ! Despite its shortcomings, it is quite a remarkable piece of engineering, truly.