House MD. : Is he using his cane on the correct side ?

House MD. : Is he using his cane on the correct side ? (hint: vascular infarct to the quadriceps muscle)

*disclaimer: Note to listeners…. there is controversy over the lyrics, there always has been and always will be …..but they are listed below at the end of the post.)

When can you ever go wrong with AC/DC ? Combine that with Hugh Laurie from HOUSE MD and you have a great mix.

So, watching this video, why is he using his cane incorrectly? We all know that House’s has a problem with the right hip and leg. “The Rules” state that with a hip problem the cane should always be used on the opposite side to change the D2 lever arm (great lesson on this: After watching this Gait Guys videos you will clearly understand (perhaps to a better level than most of your therapists and doctors who gave you the cane) why it is used on the opposite side.

So, why in the world is the brilliant Dr. House using it on the same side ? We have received this question more than once. And the answer is quite simple. His problem is likely extracapsular. In the pilot episode of House MD it was explained that he suffered a vascular infarct to the quadriceps muscle. Like bone infarcts, muscular infarcts can be painful. If he contracts the quadriceps when loading the leg there will be pain. Just like if the infarct were osseous, the loading of the cortical bone and stress on the trabecular infrastructure in that case, axial loading of the limb (muscular or osseous) will drive pain. So, to lessen the issue he uses the cane on the same side to literally share his body mass load over the length of the cane and splinting of his body mass through that right arm and the cane. He is essentially attempting to use the cane as his weight bearing limb, same as if using crutches. The cane use on the opposite side is best used when you are attempting to unload the muscular compressive forces across the hip (acetabulofemoral) joint. Contraction of the gluteus medius generates the greatest joint compressive loading of all of the hip muscles because of its orientation during gait. Thus, utilizing the cane on the opposite side acts as a hydraulic lift necessitating a shift in body mass closer to the joint and reducing the compressive demands on the gluteus medius muscle.

* Rule breaker: sure, you can still use the cane on the same side to reduce the gluteus medius forces, it is just a bit more awkward and arguably less efficient from a physics persective. But it can be done. Think about and elderly folk who had a weaker opposite arm, they would feel more comfortable using House’s strategy. The rules are not hard pressed.

* So, House is using the cane correctly for his condition. Of course, he is no dummy !

Rules are meant to be broken. When you are as smart as House you know when to break the rules.

Thanks for the reminder AC/DC ……lyrics

“Living easy, living free
Season ticket on a one-way ride
Hey Momma, look at me

Video Gait Case: Hip pathology

Video case:
another gait case from downtown Chicago. Pathology is all around us, if we are looking for it. Hopefully you are as tortured as we are.

-torso lean over the likely painful right hip (this is a compensated Trendeleburg, as opposed to an uncompensated, know the difference !)
- which side would a cane be best used on ? right or left ? (answer" left)
- she is carrying her purse on the wrong shoulder, it should be in her right hand, reducing compressive demand on the gmedius. The more the gmedius has to contract, the more compression it creates across the joint line, and if the hip is OA, it will create more pain). A cane and load in the right hand will passively manage the loads rather than actively doing it through the gmedius contraction and compression.
- heavy plunking down on the left leg. (careful not too much quad tone is developing, it can create some PF joint compression and aberrant loads and render left knee pain, that is the last thing she needs).
When you are walking about the world, play the game.
See it, and quickly gather the info, and sharpen your clinical reason skills. Get these concepts down, so you do not have to think through them in the clinic, instead, you just goto work fixing them.
If you tried to ease her burden with a sole lift (dont be a fool and use a heel lift), which side would it help her most on ? Answer: left.

Simulated knee flexion contracture to elucidate knee-spine syndrome

When we have on one side either a:
- fixed knee flexion deficit
- weak quadriceps mechanism
- short quadriceps-hip flexor complex with anterior pelvis predominance

Screen Shot 2018-01-26 at 9.16.29 PM.png

. . . these often present functionally as a short leg on that side. Perhaps better put, these will cause a premature forefoot loading response. This loading response will expedite ankle rocker during the stance phase of gait. This will often result in an overactive calf muscle complex and thus shortness over time, further blunting the ankle rocker during tibial progression over the ankle.
Furthermore, there will be a heavy lurching loading response on that same leg, it will surely look like a short leg, functionally. This is why it is imperative to check for full knee extension, ability to engage the quads with endurance and strength in full extension, and be able to connect that anterior chain with the lower abdominals and hip flexors without dumping into an anterior pelvis posture.
The loads move. They move up and down. There are many other causes of this descriptive mechanical chain problem above. Even a weak anterior shin compartment will cause many of these abrupt forefoot loading responses (that can also functionally resemble a knee flexion contracture) and promote early and excessive knee flexion during early limb loading response, when we rather should be posturing over a more stable and extended knee. They feed off of each other. It is why these syndromes of problems get intermixed and complicated to both diagnose and remedy.

PS: we chose this photo for a reason today, because high heels make us load the forefoot prematurely during the gait cycle, and we have to dampen the loads with the quadriceps.

Take what you will from this study, but it is really the global picture it suggests. That being, everything can affect everything.
PS: we hate the name they put on this study at the end. . . . "Knee-spine syndrome". For what its worth.

"However, the 30 degrees (simulated knee) contracture significantly changed the kinematics in each of the following planes. In the coronal plane, the trunk tilted to the contracture side in standing and walking. In the sagittal plane, posterior inclination of the pelvis in standing significantly increased. In addition, anterior inclination of the trunk and pelvis during walking significantly increased. In the axial plane, trunk rotation to the unaffected side significantly decreased during walking. The vertical knee force in the contracture limb decreased, being accompanied by the increase of the force in the unaffected limb during standing and walking. Results of our study suggest that knee flexion contracture significantly influences three-dimensional trunk kinematics during relaxed standing and level walking, and will lead to spinal imbalance. These facts may explain the onset of the "Knee-Spine Syndrome".

Gait Posture. 2008 Nov;28(4):687-92. doi: 10.1016/j.gaitpost.2008.05.008. Epub 2008 Jun 26.

A gait analysis of simulated knee flexion contracture to elucidate knee-spine syndrome.

Harato K1, Nagura T, Matsumoto H, Otani T, Toyama Y, Suda Y.

Pod 133: Two Gait Cases & their Gait Rehab

Today we discuss a few cases we have seen.  We discuss 2 cases, both involved poorly adapted gaits from injury, adaptations that had become the client's new norm. Once you get past Ivo's case presentation, which is very in depth, the discussions quickly go into very important topics that we all over look, namely gait and gait rehab, gait thresholds, metabolic thresholds, cortical fatigue, and how to use some neurologic principles to restore a problematic gait.

Key Tag words:
gait, concussion, head trauma, cortical fatigue, endurance, strength, gait analysis, gait problems, gait rehab, running, running injuries, run-walk, SCFE, slipped epiphysis, femoral growth plate, hip stress fractures, growth plate injury, hip dysplasia, limping gait, club foot, step length, stride length

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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.
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.

Who’s driving the compensation, anyway?

We often look at folks gait and see a pelvic drift or lean to the weak side and think “I should help them strengthen their gluteus medius”, which is often needed, but we need to think of what is driving that compensation.

Take a look at this gent that presented to the office with low back pain and watch his gait. 

Some things we hope you see are:

  • lean to the right during right stance phase
  • increased arm swing on the left
  • increased progression angle of the foot on the left
  • increased arm abduction on the left, adduction on the right
  • increased finger flexion on the left
  • slight head tilt to the left
  • tibial varum
  • crossover gait

Perhaps you are thinking, in the same order as above:

  • weak glute medius on left or QL on right or compensating for LLD on L
  • using L arm to try and help propel himself forward
  • increased balance requirements on the left so the “kickstand” foot
  • moving center of gravity the left
  • increased flexor tone to try and compensate for a weakness
  • moving center of gravity to the left, the brain needs to help keep the eyes parallel to the horizon
  • tibial varum and perhaps a more supinated foot posture, or increased forefoot pronation requirements
  • crossover

..or maybe you are thinking of something else?

The truth of the matter is that what is driving the largest part of his compensation is in fact a disc herniation, but not for what you may be thinking. The herniation is on the LEFT SIDE and at L3-L4. Take a look at the MRI Image. Yes, there is also a small herniation that L5-S1 but it DOES NOT occlude the foarmen nor hit the individual nerve roots and is on the LEFT (which you are hopefully thinking would cause left sided weakness)


So what is driving his compensation is actually a LEFT SIDED quad/adductor weakness (the femoral and obturator nerves are from L2-4). Go back and watch the video again. Can you see it?

Someone needs to be driving the bus. Don’t be too quick to jump on it until you know who is driving it and where it is going. 

A marathon a day, for over 120 days…..on one leg, battling cancer.

So you think you are tough ? This guy was tough. A marathon a day for over 120 days…..on one leg, battling cancer. 

Rest in Peace Terry. You are not forgotten. You made a mark on my life, thank you for that. Watching you skip on the good leg, giving your prosthetic enough time to swing through mesmerized me, the biomechanics of it all. If i look back, this was the first time I payed attention with great detail to someone’s gait. I was in awe, you moved me, your mission moved me, your heart and spirit moved me. Your life made a difference in mine, so I may help others.Dr. Allen
Today, June 28th, every year here on The Gait Guys, I remember Terry Fox. Every year I post a reminder of perhaps one of the toughest dudes who ever lived. Today , this day, 1981 Terry Fox died. I grew up in Canada. I was barely a teenager when Terry began his plight, The Marathon of Hope. 

His mission, 26 miles a day, every day, until he had crossed the expanse of Canada to raise awareness for cancer. He made it an amazing 120+ days in a row, 3339 miles, one one leg, before his cancer returned. The whole country stood cheering watching him do something no mortal man would attempt, let along with one leg, and cancer. Today we pay a tribute to this true rockstar.
Let this video move you, just in case you think you are having a rough day.

Difference between adult and infant gait compensation.

We highly doubt the infants compensated to the point of “recovering symmetrical gait”. It just isn’t possible seeing as there was frank asymmetry in leg length. However, it is quite possible they accomodated quicker with a more reasonable compensation, that MAY have appeared to have less limp. We did not do the study, but over a beer we might guess that the investigators might agree that our verbiage is closer to accurate. None the less, cool stuff to cogitate. We are very appreciative of this study, there is something to take from this study.

“The stability of a system affects how it will handle a perturbation: The system may compensate for the perturbation or not. This study examined how 14-month-old infants-notoriously unstable walkers-and adults cope with a perturbation to walking. We attached a platform to one of participants’ shoes, forcing them to walk with one elongated leg. At first, the platform shoe caused both age groups to slow down and limp, and caused infants to misstep and fall. But after a few trials, infants altered their gait to compensate for the platform shoe whereas adults did not; infants recovered symmetrical gait whereas adults continued to limp. Apparently, adult walking was stable enough to cope with the perturbation, but infants risked falling if they did not compensate. Compensation depends on the interplay of multiple factors: The availability of a compensatory response, the cost of compensation, and the stability of the system being perturbed.”- From the Cole et all study (reference below)

- thoughts by Shawn Allen


Infant Behav Dev. 2014 Aug;37(3):305-14. doi: 10.1016/j.infbeh.2014.04.006. Epub 2014 May 20.Coping with asymmetry: how infants and adults walk with one elongated leg.Cole WG1, Gill SV2, Vereijken B3, Adolph KE4.

The weeping calf and the deconstructed arm swing.

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

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

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

Absent right arm swing. 

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

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

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

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

Shawn and Ivo, The gait guys

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

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

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

What you should see here:

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

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

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

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

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

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

Shawn and Ivo

* remember: by clicking on the YOUTUBE logo in the lower right you will be immediately linked to a larger viewing screen on youtube.

This is a video case of a triathlete who presented with left calf pain and right quadriceps leg pain after months of training. In the video we discuss altered ankle rocker (dorsiflexion), lower crossed syndrome, altered arm swing patterning, unilateral quadriceps tightness and several other functional gait pathologies with this case.

Yesterday’s Video Case: The Gaits of Hell

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

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


in this video we see the following:

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

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