Knee hyperextension? Or does this photo suggest something more ?

You walk into the exam room and see a patient standing there just like this, What thoughts immediately flood your head ?
For me, I quickly start to juggle some things like, this:

Screen Shot 2019-05-16 at 2.53.10 PM.png

- anterior-meniscofemoral impingement ? Are his first words going to be knee pain ?
- tibial tuberosity/osgood type traction issue due to quad dominance? Are his first words going to be knee pain?
-loss of ankle rocker? Are his first words shin pain or plantar foot pain?
- tibialis posterior tendinitis ? Is he going to point to the medial ankle gutter or lower medial shin as his pain area?
-likely anterior pelvis tilt (hence weak lower abdominals), weak glutes, low back pain ?
-hamstring tightness, cramps, pain, posterior knee pain?

Just rambling real fast this morning after seeing this picture on an old hard drive.
Train your brain to think fast, think of possibilities top to bottom, don't wait for your patient to tell you where their problem is.
I play this game when i ask all my patients to walk to the back of the office to my exam room. I am watching, thinking, mental gymnastics.
Our jobs are to solve puzzles, put meaningful pieces together, to solve problems.
I use the analogy of building a puzzle. You open the box, search out the straight peripheral edges, then clump together colors, patterns. Your history and examination and gait observation should be about a process of putting together the most likely clinical picture and puzzle. And then you start to execute. Sometimes you have to walk things back, but you have to start somewhere.
But, if you wait until you get into the room, wait for the patient to say, "anterior knee pain" to start your thinking, it is easy to get tunnel vision and forget all of the other possible pieces of the puzzle that might be playing into that anterior knee pain.
REmember this, how your client moves , poorly or well, is not the problem, it is just how they are moving with the pieces and patterns available to them or how they are avoiding patterns that are painful. How they move is not the problem, it is their strategy. It is our job to find out why they are moving that way, and if it is relevant to their complaint.
Start big, funnel to small.

Shawn Allen, the other gait guy
#gait, #gaitanalysis, #gaitproblems, #clinicalthinking, #buildingpuzzles

Premature heel rise: Part 1


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

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.

Two out of Three ain't Bad...But sometimes it is

image credit:

image credit:

“What do you mean my plantar fasciitis is due to my hip?”

I recently saw a 60 YO male patient with right-sided plantar fasciitis of approximately 1-1/2 months duration. It began insidiously with pain located at the medial calcaneal facet on the right hand side. He had localized tenderness in this area with some spread distally towards the metatarsal heads. He has ankle dorsiflexion was relatively symmetrical with mild impairment on the right compared to left but only approximately 2 degrees. He had hip extension is 0 degrees on the affected side and 10 degrees on the affected side. Sacroiliac pathomechanics were present as well with the loss of flexion and extension. He had a slight leg length discrepancy, short on the symptomatic side.

So what is going on?

Moving forward in the sagittal plane requires a few things:

Adequate hip extension

Adequate ankle dorsiflexion

Adequate hallux dorsiflexion with an intact Windlass mechanism

He has a diminished step length going from right to left. Because of the lack of hip extension, the motion needs to occur somewhere. His ankle dorsiflexion is almost sufficient but less sufficient on the right (symptomatic) side than it is on the left. He has adequate hallux dorsiflexion but lacks adequate hip extension. Like the song goes, begin "Two of of three ain’t bad". However in this case, it is bad. He has an intact windlass mechanism. In fact, a little too intact. This is causing a tug at the medial calcaneal facet, creating an insertional tendinitis that we know as "plantar fasciitis".

So we did we do?

  • Manipulated the right sacroiliac joint

  • Gave him lift she/spread/reach exercises

  • Gave him shuffle walk exercises

  • Worked on hip flexor lengthening

  • Treated the plantar fascial insertion locally with acupuncture and laser therapy

Dr Ivo Waerlop, one of The Gait Guys

#gait, #gaitanalysis,#thegaitguys, #anklerocker#halluxdorsiflexion, #plantarfascitis

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

When the boot is the cause of your client's problems/pain.

Our Patreon site is LIVE.
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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."

Our Websites:

Our website is all you need to remember. Everything you want, need and wish for is right there on the site.
Interested in our stuff ? Want to buy some of our lectures or our National Shoe Fit program? Click here ( or and you will come to our websites. In the tabs, you will find tabs for STORE, SEMINARS, BOOK etc. We also lecture every 3rd Wednesday of the month on We have an extensive catalogued library of our courses there, you can take them any time for a nominal fee (~$20).

Our podcast is on iTunes and just about every other podcast harbor site, just google "the gait guys podcast", you will find us.

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

Try THIS at home...

Screen Shot 2018-02-07 at 11.23.24 AM.png

Cool test, results you can see and some literature to back it up. If you are interested at all in proprioception, this is an interesting read.

So, the question for us is: "Does ankle dorsiflexion actually create more stability, like is purported?"

“The point is that if I make their ankle rigid this way, then they can more effectively use the balance mechanisms at their knees, hips, and proximally, because they’re on a stable base. My proposition is that their balance is actually normal, apart from that distal segment. When their ankle is stabilized, they use their knees more effectively, and they become less dependent on their eyesight to maintain their balance.”

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

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.

Video Gait Case

Video Case: Another 2 minutes of chatter inside Dr. Allen's brain.
Great case, idiopathic toe walker since childhood, WITH CORRECTION.

What is amazing here is how "soft wired" this pattern is in this case. Usually toe walking is quite hardwired ("search" our blog for Primitive Toe walking) and very difficult to change if one is even extremely lucky. This case was very malleable and immediately changed by conscious effort, with zero queuing. In this case, the mere verbal queue "scuff some imaginary mud off your heels" drove him into ankle dorsiflexion and ankle rocker patterning.
Cases are sometimes about finding out if the client has the working parts, biomechanically, and the neurologic awareness and wiring to even implement a different pattern. This is a classic case of, "we do what we do"; we can get used to, and accustomed to, anything especially if there is no consequence. We can learn any habit, right or wrong. That is the beauty of the nervous system; it will learn anything you teach it, right or wrong. It is also why we worry so much. Why worry you ask ? Because everyday on this earth, some trainer, doctor, therapist, coach etc is telling their client to change they way they are doing something, whether that is "take a longer stride" or"swing the right arm more" or, "turn the left foot in more". The brain will adapt. The question is, are you fixing your client, or just asking them to compensate around their compensation, rather than fixing the underlying rooted problem ? This requires "facts, knowledge, wisdom and then insight", in that order (thanks #neiltyson).
Great case, a "Soft wired" toe walker, with immediate change in seconds. He had all the mechanical parts and neurologic wiring and ability to adapt to another locomotor pattern. Sometimes all we need to know is how to do something the right way, if you have the working parts and neurology to do so.

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

Ankle Rocker Revisited....

How many times have we talked about ankle rocker and its importance? So how are YOU measuring ankle rocker? Are you looking at it on the table? On the ground? Weight bearing? Knee flexed or extended (or both?). The knee is extended at initial contact, flexes through midstance, extends at terminal stance and pre swing and flexes again during swing phase until extending at the end of terminal swing for initial contact again.

What you see on the table may not (and many times doesn't)  translate to real life. Someone with limited ankle dorsiflexion non weight bearing may have normal amounts during gait and vice versa. With gravity in place and a functioning (or malfunctioning) vestibular system, things can change rapidly. Remember that the vestibular system drives the extensors and if inhibited, you will often have flexor dominance. Talk about a tight gastroc/soleus group!

"These findings indicate that nonweightbearing and weightbearing measurements of ankle DF PROM with knee extension should not be used interchangeably and that weightbearing ankle DF PROM with the knee extended is more appropriate for estimating ankle DF during gait."

Kang MH, Oh JS. Relationship Between Weightbearing Ankle Dorsiflexion Passive Range of Motion and Ankle Kinematics During Gait. J Am Podiatr Med Assoc. 2017 Jan;107(1):39-45. doi: 10.7547/14-112.

"There is no relationship between a static diagnosis of ankle dorsiflexion at 0° with dorsiflexion during gait. On the other hand, those subjects with less than -5° of dorsiflexion during static examination did exhibit reduced ankle range of motion during gait."

Gatt A, De Giorgio S, Chockalingam N, Formosa C. A pilot investigation into the relationship between static diagnosis of ankle equinus and dynamic ankle and foot dorsiflexion during stance phase of gait: Time to revisit theory? Foot (Edinb). 2017 Mar;30:47-52. doi: 10.1016/j.foot.2017.01.002. Epub 2017 Feb 6.


Podcast 121: Carrying things, Overtraining Syndrome, Ankle Rocker and more.

Key tag words:  OTS, overtraining, carries, carrying babies, ankle rocker, foot types, forefoot supinatus, forefoot varus, ankle sprains, nervous system, mitochondria, motor patterns, fatigue

Show links:

Show sponsors:

www.thegaitguys.comis all you need to remember. Everything you want, need and wish for is right there on the site.

Interested in our stuff ? Want to buy some of our lectures or our National Shoe Fit program? Click here ( or and you will come to our websites. In the tabs, you will find tabs for STORE, SEMINARS, BOOK etc. We also lecture every 3rd Wednesday of the month on We have an extensive catalogued library of our courses there, you can take them any time for a nominal fee (~$20).
Our podcast is on iTunes, Soundcloud, and just about every other podcast harbor site, just google "the gait guys podcast", you will find us.

Show Notes:

1. Why women carry babies on their left side
- perhaps a transition talk into arm swing symmetry, and built in asymmetries in peoples gait

2. OTS: Overtraining syndrome
this post got many hits
- CNS sympathetic-parasympathetic talk again, homeostasis

3. Chris Beardsley   Strength and Conditioning Research
From posts: December 24, 2016 , Nov 24, 2016

4. The ankles have it:

5. Foot types and knee arthritis:
The Association of Forefoot Varus Deformity with Patellofemoral Cartilage Damage in Older Adult Cadavers. Lufler, Stefanik, Niu, Sawyer, Hoagland, Gross

6. Fatigue and motor patterns:

7. Forefoot loading:

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

When the ankle lies to you

When the ankle lies to you.
Yesterday I saw something I see quite often. It was a client with dorsal foot pain, nothing shocking. But, this client had plentiful ankle dorsiflexion on the table during examination but when they walked, there was barely any use of ankle dorsiflexion-ankle rocker. Heel rise was premature.

It once again proves that just because you have it, doesn't mean it is available to be used. There was adequate hip extension and glute strength so it wasn't coming from there, though that is a frequent source. The examination was detailed, but to keep it brief here today, this client, had decent strength about the ankle from what could be determined, but they failed the hop test, control was terrible, and they could tell. Once again, if you cannot control the joint under load, the body will often not give you the full range, merely out of self preservation mode to protect the joint. This client was attempting to get more ankle rocker motion via arch collapse and over pronation to get the tibia to progress forward enough for normal gait. The collapse was causing a dorsal impingement on the foot. Lots more to come on these ideas in future posts. 
None the less, it is a good lesson to all those people out there that think that everyone just needs more ankle rocker strength and range of motion. The truth is, not everyone does, and forcing it in some will cause them pain or problems or compensations . . . . and that is your fault if it is the case.

-Dr. Allen