Normal walking and running have a certain degree of vertical oscillation, but we do not want too much

Normal walking and running have a certain degree of vertical oscillation, but we do not want too much, we want the body to move along mostly horizontal path but we do need some dampening of impact loads. We do not want to waste too much energy bouncing up and down. This is mitigated quite a bit by hip and knee flexion, the knee is well positioned to do this the easiest in many cases. Pronation and ankle dorsiflexion do dampen loads as well.

Ivo and I just recorded a class on leg length discrepancies. Here are some factors to keep in mind if there is even the smallest leg length discrepancy, anatomic or functional.

-the short leg may hyperextend at the knee , externally rotate at the hip, as well as supinate the foot (this supination is relative ankle plantarflexion, which can set up increased protective tone in calf complex and reduced strength and exposure to anterior compartment).

-the long leg side may knee flex , internally rotate at the hip, and as well as pronate at the foot (this is relative ankle Dorsiflexion)

Both of these scenarios can be going on at the same time on either leg, or it can be only on one leg. We are not perfectly symmetrical organisms, so these things can set up to help us run and walk more effortlessly, to compensate to get the head and neck properly positioned (normalizing the visual and vestibular centers on the horizon) for balance and movement through the 3 cardinal planes, and to compensate around challenging anatomy or biomechanics.

This is a complex machine, with infinite abilities to compensate and cope. But what we see is the compensation, not the problem. The joint range losses in one joint, the excesses in another, the weakness in one area, the over protection in another, the failure to tolerate loads in another, are all ways of coping and keeping us moving, . . . . . . but sometimes at a cost. . . . . pain.

shawn and ivo, the gait guys

A foot bump. What might this be, and mean?

Screen Shot 2019-02-23 at 7.27.35 AM.png

A foot bump.
We see this kind of thing all the time. This is a fixed pes planus (flat foot). When we dorsiflex the big toe, the arch does not go up as you see in the photo. That is passive dorsiflexion, if the arch does not go up passively, there is no way you are actively going to achieve this. And, using an orthotic to "attempt" to raise this arch is not only pointless, but it is futile and it will likely cause them pain. This arch does not rise, no matter how hard you put up into it. The bump, that is the navicular bone, and its associated arthritic build up at the adjacent joints, and likely soft tissue accomodation/hypertrophy. You can't needle, ultrasound, tape, adjust or rub this bump away, so stop wasting your and your patient's time selling them that wasteful thinking. It ain't gonna happen.
This is what happens when someone earns a collapsed longitidinal arch, the 1st metatarsal no longer plantarflexes (arch up) and it becomes fixed in dorsiflexion, thus affecting the mechanics at the proximal aspect of the 1st ray complex (navicular-cuneiform-met intervals).
Why? This happened because this client has significantly compromised ankle mortise dorsiflexion, and they chose to find it at the next joint complex distally, as mentioned above. So, they are finding pseudo-ankle rocker at arch collapse? Yes, we discuss this often, more pronation will advance the tibia forward. It is not desirable, but moving forward has to occur, and some people have no choice but to find it from excessive internal rotation and pronation of the limb. And this is what happens when it happens over years. Now the deformity is painful itself in the shoe, it is a new set of problems for this client.
Can this problem occur in reverse ? Yes, a loss of hallux dorsiflexion can afford the same end result.
We have a rule, at the very VERY least, check the joint above and below the area of problem/symptom. Often you will find another piece of the puzzle causing your client's pain.

The gastroc can causse ankle dorsi and plantarflexion ? Yup. What ?

The gastroc, does it cause ankle dorsiflexion and ankle plantarflexion ? Yup. What ?

You may think you know the answer, the gastrocs are ankle plantarflexors, because that is the easy one we all recognize. But I stew on things when unique cases come in and do not fit the "normal" models and it got me reviewing principles I need to always keep in mind.

Think about it, the gastroc cross the knee, so it causes knee flexion. And when the knee flexes, the proximal tibia is progressing forward in the sagittal plane. Now remember, the foot is on the ground, so the distal tibia is (relatively) fixated in relation to the upper tibia. So, as this proximal top tibial moves forward, because of gastroc contraction, the muscle is actually causing ankle dorsiflexion !

So, it is it important to know your normal gait cycle events ? Yes, Ivo and i harp on that all the time ! One has to know the normal cycles to know when abnormal gait cycles are presenting clues.
So, am I saying that the gastroc are helpers of ankle rocker and ankle dorsiflexion ? Yes, they can be. It is a timing thing. So, we have to again get out of our model of open chain events, and thinking that only the anterior compartment muscles are ankle dorsiflexors. We also have to remember that a bent knee heel raise is not the same as a straight leg (knee extension) heel raise. One can stimulate and assist in ankle dorsiflexion and the other cannot so much. So, in clients with loss of ankle dorsiflexion/ankle rocker should you be assessing the function of the gastroc at the proximal knee, for its effects of dorsiflexion at the ankle ? Yes. Go ahead and try it, bend knee and straight knee heel raises, they are different beasts. This gets more complicated, and i will go into that next week ! I have had some deeper epiphanies i wish to share.
Also, remember, single and biarticular muscles have varied and vast capabilities. Thus it is always vital to consider whole body movements where muscles have abilities to accelerate, decelerate, and control and stablize joints they span, and do not span, via dynamic coupling.
Dr. Allen

This could happen to you if your ankle dorsiflexors get weak.

This could happen to you if your ankle dorsiflexors get weak.

This (read below) is actually a normal compensation. Building strength on this compensation without resolving the anterior compartment weakness can lead to knee pain (or other things). It is why, again, we say that asymmetry and especially asymmetrical compensations, can matter in your client.

"muscle strength asymmetry in the ankle joint may lead to counterbalancing muscle strengthening of the knee joint to maintain the center of body mass."

"It is not only the balance between the agonist and antagonist muscles, but also the balance between the left and the right, and between the proximal joint and distal joint in a weight-bearing position that are involved during exercise. As seen in the university players in this study, the weakening of dorsiflexors due to muscle strength asymmetry in the right ankle joint is thought to cause the strengthening of the extension muscles of the knee joint in order to maintain the center of body movement and stability." - Kyoungkyu et al.

What The Gait Guys have to say about this:

As that foot is approaching the ground, and begins loading, the anterior compartment may not skillfully allow a forefoot loading response and may not protect that anterior ankle mortise joint let alone appropriate and skillful pronation. Ankle dorsiflexion loading may occur too fast and uncontrolled leading to sudden undesirable knee flexion (too much, too fast, too long). After all, closed chain ankle dorsiflexion and knee flexion are deeply paired loading movements. One way to slow down this increased amount of forward tibial progression (ankle dorsiflexion and knee flexion), is to increase the activity of the quadriceps/knee extensors. The compensation of increased knee extension loading will offset the increased knee flexion resulting in improved control the ankle dorisflexion. It is a reasonable compensation, but not one you want to stick around for long or unaddressed. If subtle, and left over time, perhaps even when subclinically presenting, knee pain from increased shear/compression or other mechanical results, may be the first presentation when the true problem is down in the lower region.

Remember, this is about controlling gait and thus center of body mass. This is about not falling over. This is about the central nervous system making necessary adaptations to protect the entire organism, which sometimes means doing anything so as not to fall. Now, just to make this more complicated and fun, imagine that this is a fairly common problem and compensation ON ONE SIDE of the body. So now imagine, the changes in arm swings, maladaptive loading onto the other side, pelvis asymmetry and the list goes on.

Of course, one could just globally add strength to this client, such as more squats, lunges or more deadlifts (instead of a focal intervention at the anterior ankle structures) thus adding another layer of compensation, and perhaps making them feel better, for the time being. Essentially, adding global strength to asymmetry. But make no mistake, this problem is likely to sit here and percolate under the surface with more possible compensations, subtle movement alterations and adaptations, until someone addresses the problem. And remember this, if one does those things long enough, those become a client's new adaptive neuroplastic patterns. Strength first is not always a good first intervention.

J Phys Ther Sci. 2016 Apr; 28(4): 1289–1293.
Effects of muscle strength asymmetry between left and right on isokinetic strength of the knee and ankle joints depending on athletic performance level
Kyoungkyu Jeon, PhD,1 Sungyung Chun, PhD,2,* and Byoungdo Seo, MS, PT3

photo credit: free photos courtesy of Pixabay

Podcast 137: Running: Limitations in thoracic spine function matter

We cover many aspects of human movement on this podcast, the topics are broad ranging on today's show, but they are worthy of your time in our opinion.

direct download:



Key words:
arm swing, thoracic extension, scapular retraction, arch height, rear foot posting, forefoot loading, ankle dorsiflexion, ankle rocker, shoulder extension, SSEP, F-wave, EMG/NCV testing, gait ataxia
Here are some key quotes from today's show:

You may have the range of motion, but are you actually able to use it?
You haven't truly injured yourself, you've just lost your ability to compensate.

And we discuss a case study today, where the following paragraph is germane.

"Abnormal gait changes might be the first signs of an early slow cooking neurologic disorder. Most, not all, pathology is afferent, yet most (not all) EMG/NCV testing is geared towards the efferent pathology (motor end organ disease, not sensory compromise), hence, testing can miss your client's pathology.  We discuss a classic case where the client clearly had the beginnings of a neurologic disorder on our exam (clonus and joint position sense changes and clear ataxic gait) yet the testing "that was done" showed a normal study of this client.  Much pathology is afferent, the input is the problem, so you need to consider requesting Sensory nerve action potentials, SSEP and F-wave testing, because they are difficult to elicit and good technique is paramount. Hence these extra components of the test are not done, and you need to ask for this in your testing.  "Maybe it's not there because you are not looking".  We have much more on this topic, come listen to Podcast 138 and get the full monty."

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Our website is all you need to remember. Everything you want, need and wish for is right there on the site.
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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

Have impaired ankle rocker or ankle dorsiflexion ? Try out these shoes.

Have impaired mid or forefoot rockers?

This will come to little surprise to anyone who has been here awhile at TGG. But I finally got around to putting on a pair of the HOKA Bondi 5 recently and boy was I surprised how much rocker was built into the forefoot. I can now see why there is such a dramatically beneficial response to patients with a painful hallux joint complex. I had been in their Claytons and Cliftons before to trial them out, but never a pair of Bondi 5's.
If you have a client with impaired mid to late stage ankle rocker or forefoot rockers (there are 3 rockers, Heel Rocker, Ankle rocker, and Forefoot Rocker) this shoe will buffer the loads. It is no replacement for attempting to remedy biomechanical faults or limitations, but , if you have a client where solution is not available and management of loads i the only way, then this shoe will be a gem to you and the client. Go try a pair on so you know what we mean. The rocker is massive and effective, and one might argue, a little excessive (but we are not complaining). The Dansko clog can be another alternative for some clients.
Changes in running kinematics and kinetics in response to a rockered shoe intervention.
Boyer KA, Andriacchi TP.
Clin Biomech (Bristol, Avon). 2009 Dec;24(10):872-6. doi: 10.1016/j.clinbiomech.2009.08.003. Epub 2009 Sep 9.

Hoka Bondi or Dansko Clog

Lumbar spine mechanics and boots

Your footwear can affect your hips and low back ? Yes.

If you have been with us even a short while, this study should be of zero new value to you. But this study looked at the ankle dorsiflexion restricting firefighting boots on the low back.
We know that there are several force dissipators in the lower limbs, those being hip flexion, knee flexion and ankle dorsiflexion not to forget the all important foot pronation. When one of those is compromised, the job of that joint complex typically gets shunted elsewhere, and often proximally into the body.
Obviously, above ankle boots will restrict ankle dorsiflexion. Imagine an ice skate laced up all the way, or a ski boot, the ankle dorsiflexion virtually disappears. The came can happen in an inappropriately laced hiking boot or high ankle trail running shoe.
This will hit home the posts earlier in the week on the "z-angle" we discussed and Gray Cooks video from the weekend.
It is possible if you dial back the ankle dorsiflexion you cheat hip extension, or you make the lumbar spine extend into more lordosis than it is happy to perform.
You just cannot rob Peter to pay Paul all the time. Eventually Peter is gonna get pretty pissed.…/article/pii/S0003687017301333

More on the Z-angle

More on the "Z-angle". Why your hip and ankle have to talk to each other.

We have been saying this kind of stuff for years, but in this video perhaps Gray Cook says it in a way that will resonate well with some when we can be a bit too wordy at times, Gray is always eloquent and well spoken. We often discuss this ankle and glute relationship he mentions in a topic we refer to as "the Z- angle". And, we discuss the greater global ramifications of unresolved ankle sprains. Search our blog for these terms and topics.
It is rare that our in-office therapy and our corrective home work for a client does not address both the ankle and hip simultaneously. We know this tight relationship exists, and so should you.
In many of our podcasts and blog posts we pound sand on the fact that just because you have ankle mobility on the exam table does not mean you will have it available in some movement patterns or in some of your sport movements. And, ankle functional impairments are key players in multiple injuries and impaired movement patterns. We like the "software vs hardware" terminology he uses, we will be borrowing that verbiage in the future, it is a nice way to tighten up a dialogue without getting wordy. Great job as always Gray !

Video case: Ankle dorsiflexion ? Um, maybe, maybe not.

The more i talk to people about ankle rocker and ankle dorsiflexion, the more i realize they just do not have all the anatomical understanding behind it. But how does one apply the concepts if they don't fully understand it ? It is baffling.
The client should be assessed both passively and actively. When you look at someone's ankles during their gait, do you look at the knee response at ankle dorsiflexion  or at heel rise or during forefoot loading? Do they momentarily hyperextend the knee? Flex the knee? Rotate the foot or leg internally or externally ? To they prematurely heel rise ? Do they prematurely unload the limb and lurch to the other limb thus shortening step length? Do they progress strongly to the lateral forefoot during loading or do they find a middle ground and begin the pronation phase timely with a proper progression to the medial foot tripod ?  Remember, what you see is their strategy, not their problem, do not correct what you see, correct the cause of what you see.

In this video, look at the excessive right knee flexion that occurs here during active ankle dorsiflexion. One must understand what this could mean, and then should be able to see some of the causation during gait. One of the calf complex muscles crosses the knee, one does not. One of them is short on this right side in this client with acute achillies tendonitis. It is not necessarily the cause, but it a piece of the puzzle. Both the clinician and the client do not realize that there is often a knee flexion response during active and passive ankle dorsiflexion assessment, especially when there is mechanical pathology. Having a foam roller under the knee can really bring it out, as in this case. But, remember, this should not be the standard of your assessment, because you are putting slack into the posterior mechanism.

So you say your client needs more ankle rocker? Faking out ankle dorsiflexion and ankle rocker.


I was reminded again yesterday, after yet another foot pain client came in to see me, that many do not understand the absolute and deeper ramifications of putting an orthotic into a shoe (and onto a foot) and what effects of doing so can have on changing a necessary adaptation.

This client had medial heel pain, not plantar heel pain, not the posterior calcaneal area, the medial edge (see photo). The edge where the inside/medial edge of the calcaneus/heel meets the ground. This client could reproduce the pain on palpation and could reproduce it if they stood up, and everted the heel just a tiny bit.

This client had a healthy appearing foot and arch. But, as often is the case, appearances are deceiving. 

Here was the major problem:

- client had loss of terminal ankle dorsiflexion from prior fracture immobilization


- top end calf weakness * (see later)

- client had clear fatiguability of the anterior shin compartment muscles, and mild toe extensor weakness

- the client had high arched supportive orthotics

So, what is happening here, and often happens with the above limitations, the client does not have the muscular ability to maintain the arch sufficiently from the big players, as noted. In other words, the ankle has lost mobility and the foot has lost stability, a common pattern. To make up for a loss of ankle dorsiflexion we often collapse the arch a sufficient amount to pitch the talus medially and forward to help the tibia progress forward the requisite amount needed for forward locomotion across the foot-ankle complex. This is a normal compensation, and in time there may be a pathologic cost. This medial approach of the talus and arch collapse, requires calcaneal eversion. This eversion means more medial calcaneal loading into the shoe, orthotic or ground, including medial soft tissue (mostly fat pad) loading between the ground and the everting calcaneus.  

This is a normal compensatory strategy to move forward over a restricted ankle dorsiflexion range. However, the doctor this client saw previously (for plantar fascitis), felt that this motion was a problem they needed to block with an orthotic. One that resisted the heel eversion and more than normal arch collapse/pronation cycle. This remedy resolved the plantar fascial pain. But, the medial heel pain began shortly thereafter. 

So, here we have a client that is compensating, and finding a way (though there are biomechanical costs to this way), to get past a limitation, loss of ankle rocker in this case. But, the doctor put an orthotic in the shoe that stopped this "way".  Now the client has to evert the heel even harder, because of the presence of the orthotic preventing it) and it is causing a "bite" or friction plus compression of the medial soft tissues. 

So, this client now still cannot compensate well, in the manner they have attempted to do so, because of the orthotic. So, where are the loads going to go now ? Yes, some are being rammed into the medial aspect of the orthotic, but some are likely going to so elsewhere. Remember, the client is trying to progress their mass over and past the limited ankle rocker, and more pronation was their strategy. But, the orthotic is preventing that.  So, the loads are very likely going to move up the chain (because the orthotic is muting loads down into the foot). 


Me:     "Oh, wait, "Mr. Jones", didn't you say you were just recently beginning to have some posterior knee pain ?  Let me tell you why you are hyperextending your knee a little more than normal and taxing out your gastrocneumius.* One way you can progress forward, if you cannot do it through ankle rocker, is to extend your knee a little by contracting your quadriceps a small amount at midstance.  Lets discuss why the orthotic is not helping you, not solving your problem, and creating some new issues for you. Then lets get down to fixing the root problem."

Some things to think about.  Orthotics are not bad, but the user has to know when they are a device to help a client progress through a problem, and when they are inappropriate. Not all increased pronation is bad, particularly when it helps a client get through a problem. But, fix the root problem, and then help them regain proper amounts of pronation.

Oh, and one more thing, all you "drive more ankle rocker and dorsiflexion" people out there. Are you driving more ankle dorsiflexion, or are you merely pressing the talus into more medial posturing, plantarflexion and adduction? These are the talar motions in pronation. And when you pronate, you get more ankle rocker, faked out ankle rocker. So, are you truly helping your client get more ankle rocker and dorsiflexion ? Is this increased pronation what they are doing during their squats, to "apparently" get enough ankle rocker/dorsiflexion?  Be careful all those new found ankle rocker mobility drills are not just making your client pronate more than normal. We know it happens, we see all the time. Loss of ankle mobility and loss of foot stability are often a paired phenomenon, they are trying to talk to you and tell you to treat the root cause.

-Dr. Allen, one of the gait guys

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.


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. 

Ankle stiffness and foot collapse, correlation ?

A client who comes in with calf tightness and ankle stiffness can't be clumped into the catch all group that they need more ankle rocker or to just stretch out the posterior mechanism.

Screen Shot 2017-03-02 at 7.57.05 AM.png

In all likelihood they probably don't have a stable enough foot/arch and are passing their body mass over that unstable structure, collapse ensues before ankle rocker is completed during stance phase of gait. Thus, the body goes into a strategy the next joint complex up the chain and attempts to gain stability at the ankle complex and the most available tools, the posterior mechanism. The foot should be stable and the ankle should be mobile through sagittal ankle rocker. When the foot is unstable, things often switch; the once mobile ankle rocker shifts towards stability attempts. Not everyone needs ankle rocker work ! Don't force it, make them earn it once you find the root of the problem. In a huge chunk of the population, that stiffness and loss of ankle rocker is there as a coping mechanism to find stability. Don't take it away from them ! 
PS: raising someones arch with an orthotic doesn't earn any stability, it is borrowed, it is false, so keep that in mind. Not that it doesn't have value or a purpose, but nothing has been intrinsically fixed, only extrinsically and that cannot be forgotten. Someone has to pay for these loads coming into the system.
-Dr. Allen's rant of the day

Varus Thrust Gait, Trampoline ankle Part 2: When ankle rocker is lost.

In several previous case videos we have shown a case of traumatic ankle injury causing ankle rocker loss and subsequent knee hyperextension during sagittal gait progression, and we have shown a case of a classic Varus Thrust gait (search our site).

Today, I will shows you a case where the 2 phenomenon are connected. If you know your normal anatomy, you should be able to put this together.

Case background, video #1:  *Impaired ankle rocker (severe) in action. This was a case of ankle talus dislocation while trampoline'ing :) No surgery, but ankle was bagged up for 6 weeks. This is a TIGHT and blocked ankle rocker now, better for it to be more stable than unstable since every ligament was torn completely. These are his first steps in 6 weeks. 90 ankle dorsiflexion on the table, which is insufficient for anyone to have normal gait. Here is a great view of what happens when there is insufficient ankle rocker, one scenario at least (there are several ways around an insufficient ankle rocker). Here you can see the knee hyperextension strategy at the moment the body mass attempts to pass over the ankle, the ankle says "Nope, not today bud, try throwing the knee into extension to get over me.". And so, that is what happens here. Imagine what message the hip and glutes get from that strategy ! So, you won't see this every day, but imagine all the cases of minor ankle rocker impairment you do get in a few of your clients, and the micro knee extension strategies you can't see, that are fiddling with optimal mechanics. If you do not look, you will not find. It is why I mentioned the case last week of the ankle ROM looking normal on the exam table, but it not being used during gait. Again, not everyone needs more ankle rocker, often they need more S.E.S. (skill, endurance, strength). Skill includes, proprio, balance, coordination, motor patterning, etc. Make no mistake, this fella needs more ankle rocker !

in the sagittal video below, and more obviously in a separate video further below to more clearly demonstrate a more classic Varus Thrust gait, one should be able to see the knee undergoing a sudden abrupt varus (lateral) shift during the gait loading response.  The tib-femoral joint is a sagittal hinge, not a frontal-lateral plane hinge, so this is clearly pathomechanical movement. This knee will likely undergo premature knee cartilage and meniscal degeneration if the phenomenon is not resolved.
The cause of this issue is likely more simple than complicated however there may also be multiple factors coming together in a perfect storm. However, make no mistake, in order to understand a varus thrust gait, one has to understand the why and how of the gait presentation. Additionally, one must have a clinical knowledge of the restraining systems of the knee, both active and passive, and have a high degree of clinical suspicion and working knowledge of how to assess for these types of problems. It this immediate case below, with the severe ankle rocker loss (see in the first video) the client hits the loss of ankle rocker/dorsiflexion and must attempt to move forward. In video #1 we see knee hyperextension, but what you need to see on the video below is knee varus thrust. This is a soft case, it is not a TRUE varus thrust, but the mechanism is there. It is there on that left leg/knee if you know what to look for, and is in part because he is supinating the foot excessively, while moving through neutral knee and into terminal knee extension, to try and find some kind of lateral frontal plane strategy to get around the blocked ankle rocker. Remember, there is lots of medial and lateral joint play at neutral zero degree extension, and very little if any in terminal knee extension lock out. So the shift occurs mostly around the zero degree range and then is thrusted into terminal extension giving it that "sudden abrupt" appearance. Remember the knee is not a frontal plane hinge, but it does have some frontal plane wiggle room at zero degrees, test it out for yourself !  Why does this phenomenon occur in this client with zero posterolateral corner knee injury ? Well, it is simple anatomy. The medial condyle is longer and deeper than the lateral (see xray photo below showing this relationship) and with such far lateral foot supination combined with terminal knee extension, he is likely only bearing weight on the medial condyle and the joint pivots and shifts in this zero degree extension through to hyperextension lock out (not a true instability pivot-shift but the mechanism remains present) until the LCL (lateral collateral ligament) complex and iliotibial band and other lateral structures engage. Because there is no true lateral laxity, there is only a subtle lateral shift,  unlike the 3rd video below of the lady walking on tiles. So, this is a case of knee hyperextension and mild varus thrust gait from a blocked ankle rocker motion joint. 


Below are some thoughts from a prior video on Varus Thrust gait (see video to the right). You must understand all of these components to help these clients fully. 

Things to consider:  
- old ACL/PCL and posterolateral corner damage (search our site for articles we have composed)
When the posterolateral corner complex of the knee is torn up from a blow to the knee or a torsional loading failure, the 3 components of the posterolateral corner (the lateral collateral ligament (LCL), the popliteal tendon, and the popliteo-fibular ligament complex). This complex attaches just in front of the origin of the lateral gastrocnemius tendon off the lateral femoral epicondyle. This complex can be blown out from either a PCL or ACL injury mechanism, these big player ligaments are rarely torn in isolation.
- is there a Pivot Shift phenomenon, likely.  A positive Pivot Shift test will be present. One must know how to perform this test to confirm its presence, it can be a tricky test if one does not know the load vectors to apply and what the shift feels like and where it occurs during the test. This can be a very subtle positive test, again, first hand experience is everything. 
- one must find this before surgery occurs for the ACL or PCL. Failure to find and address this damaged complex will likely result in rotational stability problems once return to play occurs. IT will not likely be noted in the initial post-operative months as the aggressive loading response will not be performed early on. Failure to address this problem will likely put ACL-PCL reconstruction success at a high risk.

Other critical factors to consider in the Varus Thrust Gait:
- is there medial knee osteoarthritis ?
- what is the foot type and what are the mechanics ?  ie. Forefoot varus, Forefoot supinatus, rearfoot variances
- does the patient have excessive pronation challenges that create massive internal spin into the tibia ?
- is the hip frontal and rotation plane stable?  Can the patient adequately control rotation at the hip level ?
- is there a Cross Over gait phenomenon with narrow based step width ? (search our blog and youtube for  "gait guys crossover gait").  A narrow step width will create an "unstacked" limb and promote more rotational risk into the limb, often playing out at the least tolerable joint to rotation . . . the knee.
- Does the client have Tibial Varum ? Genu Varum, Genu Valgum ? These can promote and complicate the Varus Thrust gait.
- Does the client have Tibial torsion or Femoral Torsion variants ? These can promote and complicate the Varus Thrust gait.

- is there weakness of the lateral gastrocnemius or biceps femoris (to name just two the directly cross over this posterolateral interval and can offer joint compression/stability ? What about weaknesses in the medial leg ? Not that these are anywhere sufficient to offset a PLRI (posterolateral rotatory instability), but, they are secondary helpers/restraints.

One should clearly see now that the Varus Thrust gait is potentially complicated and multifactorial. One MUST understand:
1. many components of normal gait and normal anatomy from foot to pelvis, at least.
2. be able to assess for aberrant mechanics and pathologies within all joints of the lower limb
3. be able to assess for post operative rotational stability and laxity (*even a healed, yet partially attenuated, Posterolateral corner complex that was not noted or addressed in the ACL-PCL reconstruction can come back to haunt even the best reconstruction. Those little rotational instabiliites will build over the years and render attenuation of the other secondary posterior restraints in the knee. Like a Lisfranc injury, sometimes things take a few years to brew and blossom before the "career ender" instability shows up. Trust us, we have seen it enough times.  

Rule: if one does not know it exists, one will miss it. If one does not know how to assess it, one will miss it. If one does not know normal anatomy, torsional variants, foot types and gait types, one is likely to be lost and left fumbling.  Our clients deserve more. 

Clinical pearl: if you are radiographically sharp, you should have noted the Pellegrini-Stieda lesion at the medial tibial epicondyle (this is not a radiograph for this case, it was used to show the longer medial condyle reach). These are ossified post-traumatic lesions near the medial femoral collateral ligament attachment. This avulsion injury of the medial collateral ligament can calcificy after a few post-trauma weeks. 

- Dr. Shawn Allen, the other gait guy

Trampoline ankle case: Part 2

Trampoline ankle: case progression:

*We have not uploaded this video to youtube yet. It is on our Facebook page on Feb 11th. Go watch it there. We will compose this case as it progresses and put together a complete video then. But you can see what is discussed below, in the FB video,February 11th.

Impaired ankle rocker (severe) in action. We showed you this case last week, the ankle talus dislocation while trampoline'ing :) No surgery, but ankle was bagged up for 6 weeks. This is a TIGHT and blocked ankle rocker now, better for it to be more stable than unstable since every ligament was torn completely. These are his first steps in 6 weeks. 90 ankle dorsiflexion on the table, which is insufficient for anyone to have normal gait. Here is a great view of what happens when there is insufficient ankle rocker, one scenario at least (there are several ways around an insufficient ankle rocker). Here you can see the knee hyperextension strategy at the moment the body mass attempts to pass over the ankle, the ankle says "Nope, not today bud, try throwing the knee into extension to get over me.". And so, that is what happens here. Imagine what message the hip and glutes get from that strategy ! So, you won't see this every day, but imagine all the cases of minor ankle rocker impairment you do get in a few of your clients, and the micro knee extension strategies you can't see, that are fiddling with optimal mechanics. If you do not look, you will not find. It is why I mentioned the case last week of the ankle ROM looking normal on the exam table, but it not being used during gait. Again, not everyone needs more ankle rocker, often they need more S.E.S. (skill, endurance, strength). Skill includes, proprio, balance, coordination, motor patterning, etc. Make no mistake, this fella needs more ankle rocker !

-Dr. Allen

* again, this video does not play, read above

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 goVERTICAL 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, oryou 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 :

Podcast 113: The Hip-Ankle "Z" angle, It is all you need to know.

Plus:  Bringing together hip extension, ankle dorsiflexion, looking at the 6 locomotion compensations to strategize around impaired ankle dorsiflexion during gait/running.

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The Circle of Durability.

The article below for some reason inspired today's soft rant. I hope you feel this is worth your time. 
Yesterday I talked about arch height and ankle mortise dorsiflexion and how we can obtain more global dorsiflexion range through some pronation, loosely meaning, some arch compression/drop and splaying apart of the tripod legs of the foot. Global arch flexibility is a piece of that puzzle.  This action of arch compression/drop/tripod splay moves the tibia forward in the sagittal plane and this is global dorsiflexion. Let me be clear however, a reduced ankle mortise dorsiflexion range of sagittal motion which is met by more arch height reduction/prontation/tripod splay, is still dorsiflexion however it is less sagittal dorsiflexion and a little more adduction and medial drift. This can bring the knee into the medial plane and it does promote more internal spin of the limb, this can be a problem.  None the less, it is still global dorsiflexion. It is something we see at the bottom of a squat, we see it because to get there most of us do not have all that dorsiflexion at the mortise. It is not abnormal, the question is, "is it safe for you? Can you do it repeatedly, safely?" It is where we go when we need more sagittal motion, but it may not be ideal, and is often what creates functional pathology. We see it all the time, someone says in an email, "I have plenty of ankle dorsiflexion, that is not my issue".  Do you have plenty? Is it not really your problem? This is fine tuning stuff, it takes a skillful eye and assessment hand. It takes experience to see the whole picture. You cannot get this full 4k experience and understanding from a 2 dimensional youtube video. This arch compression and pronation is normal to occur, it should occur, it must occur. But, how much is too much, for you ? I like to explain it this way, 

"there is a point at which sound, economical, durable, biomechanics becomes a liability. And, at that point where the liabilities begin is in fact where we begin to skirt the edges of that durable skilled movement. Where we begin juggling our liabilities is where the risks begin to mount and begin to whittle away or trump our S.E.S.P (skill, endurance, strength, power). This is where injury often occurs, at that intersection where the gas tank of our S.E.S.P. begins to run low and our liabilities begin to run high." 

I have explained this concept many times before when talking about the cross over gait. Moving towards a narrower step width is fine if you have the durability to be there. The question is, how long are you going to be there ? A cross over gait tendency is more economical but you begin to risk liabilities toward injury if that durability becomes challenged. As a runner you must know where your safe zone exists and know how much durability you have at those fringes of your movement. It is when you are there too long, too often, or too much that you empty that durability gas tank which then increases your liabilities towards injury. This is why I give high volume and strength work once a problem is solved, to make sure that they can keep that circle of durability high. It is when we stop keeping our gas tanks large and full that we run on fumes and our risks increase. You might be able to run economically for 5 miles with a narrow step width cross over style running gait. But, can you do it safely at 10 miles ? How about 15?  Is it any wonder why people get injured as they fatigue their safe motor patterns ?  If they have worked hard to keep that circle of durability large (S.E.S.P.) they are bound to be safer and less injured. Injuries occur because we exit our circle of durability, its gas tank has run too low, liabilities now trump economy and durability.

- Dr. Shawn Allen, the gait guys

Toe flexor strength and ankle dorsiflexion ROM during the countermovement jump

This study looked to evaluate the relationships between peak toe flexor muscle strength, ankle dorsiflexion range of motion, and countermovement jump height.

"The results showed (1) a moderate correlation between ankle dorsiflexion range of motion and countermovement jump height and (2) a high correlation between peak first toe flexor muscle strength and countermovement jump height. Peak first toe flexor muscle strength and ankle dorsiflexion range of motion are the main contributors to countermovement jump performance."

There could be variables missing here, and plenty of caveats. We should try to get the full text on this one to be fair. None the less, interesting facts to brain juggle however.
These muscles are posterior compartment muscles so it makes sense, however, when the first great toe (the hallux) is in relative flexion, the arch is easier to drop (conversely, hallux dorslflexion causes the arch to raise and keeps the ankle dorsiflexion more purely in the ankle mortise) where as, with relative toe flexion, the arch can drop, this can generate some pronation and arch splay, which can increase the "appearance" of more ankle dorsiflexion when in fact some could be from the arch drop/pronation. I wonder if the researchers are aware of this variable or if this study took it into consideration. Certainly when someone is dropping into ankle dorsiflexion ready to jump, is is easy to drop the arch. Go ahead, dry doing it with the toes down , and then with the toes up in extension, its very different in the amount of dorsiflexion you can get out of the entire arch-ankle mortise complex combined. IT is these kinds of things that can easily be over looked and skew findings.

Correlation between toe flexor strength and ankle dorsiflexion ROM during the countermovement jump

Sung Joon Yun1) 2), Moon-Hwan Kim2), Jong-Hyuck Weon3), Young Kim4), Sung-Hoon Jung5), Oh-Yun Kwon5)

Journal of Physical Therapy Science
Vol. 28 (2016) No. 8 August p. 2241-2244

link :