Last week we ran an archived piece named, “Just because a muscle tests weak doesn’t mean it  needs to be activated”.  Here is the link to that piece.

Today we present some more proof behind our stance on this topic. The referenced article below states in its Context: “An arthrogenic muscle response (AMR) of the soleus and peroneal muscles has been previously demonstrated in individuals with chronic ankle instability (CAI), but the presence of AMR in muscles acting on joints proximal to unstable ankles has not been previously explored.”

And here was their study’s conclusion: “Arthrogenic inhibition of the hamstrings muscles bilaterally and facilitation of the quadriceps muscle ipsilateral to the involved limb were noted in subjects with unilateral CAI. Motoneuron pool excitability appears to be altered in muscles that act on joints proximal to the ankle in those with unilateral CAI.”

This proves our thoughts on a deeper level.  Just because a muscle tests weak does not mean that this muscle is weak or “inactive” or needs  to be “activated”. It is a shame it is not as simple as finding something weak and “activating” it. As we eluded to, this is a far more complex system than that, there are complex feed forward and feedback loops that are mandated and regulated by local cord reflexes, pattern generators and complex cortical loops.  Putting a muscle “back on the grid” prior to activity merely because it tested weak may be putting your client at risk if you are not getting down to the bottom of the problem.  Taking the study mentioned here to a deeper level, finding out that your client has a weak hamstring or quad and negating the possible source of the problem down in an ankle could be devastating to an athlete if they are suddenly returned to aggressive activity immediately after being “activated”.  You may be over riding the central pattern generators, reflex responses and complex cortical loops arthrogenic responses, which could be neuro-protectively calculated. As this article mentioned, “motoneuron pool excitability appears to be altered in muscles that act on joints proximal to the ankle in those with unilateral CAI”.  This is a massively diffuse process going on constantly throughout the body, providing safe mobility and stability. It is not a random process and should not be intervened therapeutically on a random level. At the very least, it requires a patient history, clinical examination, gait evaluation and movement pattern assessment. Anything less is, well, your responsibility if poop hits the fan when they step on the field. 

Shawn and Ivo

Reference:

J Athl Train. 2007 Jul-Sep; 42(3): 355–360.PMCID: PMC1978472Arthrogenic Muscle Response of the Quadriceps and Hamstrings With Chronic Ankle InstabilityEdward J Sedory, MEd, ATC, EMT,Eric D McVey, MEd, ATC,Kevin M Cross, MEd, ATC, PT,Christopher D Ingersoll, PhD, ATC, FACSM, and Jay Hertel, PhD, ATC, FACSM

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1978472/

“Neural circuits linking activity in anatomically segregated populations of neurons in subcortical structures and the neocortex throughout the human brain regulate complex behaviors such as walking, talking, language comprehension, and other cognitive functions associated with frontal lobes.” 1

We also found this interesting quote from Science Daily on this topic of complex sensory motor behaviors and on the varying information on central pattern generators.

ScienceDaily (June 3, 2012) — “A new finding that motor cortex is a dynamic pattern generator upends existing theory with broad implications for neuroscience.”

“Maybe it is actually easier to understand than we thought. A new paper presents some compelling evidence that the motor cortex, rather than being command central, is more like a part of the machine, sending rhythmic signals down the spinal cord to orchestrate movement.”

"The electrical signal that drives a given movement is therefore an amalgam — a summation — of the rhythms of all the motor neurons firing at a given moment.” This is of course monitored (and modified) by one of our best friends, the cerebellum. 2

The cortex is where movement begins and where it ends; from areas 4, 4s and 6 in the precentral gyrus of the brain’s frontal lobe, down the spinal cord and out to the muscle through the peripheral nerve.   It is also where the information from the body’s receptors feed back,  to give updates on where the body parts are in space (proprioception) and how they are doing functionally (comparing information about length, tension, etc).  It is about sensory and motor function.  Motor function is based on sensory input.  Good motor function is based on good sensory information. It is a subtle, beautiful, intricate symphony.  And when one part goes wrong, the whole system can be thrown off.  

Here is an example we sometimes use in our lectures and with our patients to make this point clear.  Imagine an orchestra playing Beethoven’s beautiful Ode to Joy, a choral symphony for orchestra.  Now imagine one of the musicians begins to play off key. In time, the musicians sitting around that musician who are most locally influenced by that off tune musician, soon become irritated and have troubles playing “in tune”. In time, if not rectified, the whole orchestra could be corrupted and being to take that lead as well.  Hard to believe, but it makes the point that all it takes is one piece not playing well to change the outcome. Similar analogy, all it takes is one weak muscle or one painful joint and the outcome is skewed away from the optimal outcome and in time local dysfunction and compensation becomes an all encompassing compensation. The body’s function and operation, when proper, is an orchestra and orchestration with each piece doing a local job with a more global contribution to the bigger job. When all pieces come together appropriately it creates a symphony of flawless, effortless movement as seen in the video above.

Shawn and Ivo, the gait guys

refs:

1. Front Syst Neurosci. 2014 Feb 13;8:16. eCollection 2014. Cognitive motor interactions of the basal ganglia in development .  Leisman G1, Braun-Benjamin O2, Melillo R3.

Simple Foot Exercises are effective!

Conclusion “These results suggest that the toe spread out (TSO) exercise can be recommended for preventing or correcting HV deformity at an early stage.”

We know and teach that foot exercises work. Here is a nice objective paper (click underlined for abstract) on two exercises we prescribe often.

Here is our variation of the TSO exercise we call the “Lift, Spread and Reach” exercise

Stand comfortably with your feet about shoulder width apart

Stand on your foot tripod with your toes extended. Concentrate on feeling pressure at the center of the calcaneus, the head of the 1st metatarsal and the head of the 5th metatarsal

Lift your toes as high as possible

Spread out (abduct) your toes as much as possible

Reach forward with your toes as far as possible

Place your toes back don on the ground as flat as possible.

repeat 10 X

You can augment the exercise with a rubber band around the toes to provide resistance after you can perform the exercise competently.

Happy exercising!

Ivo and Shawn

Kim MH¹, Kwon OY, Kim SH, Jung DY.: Comparison of muscle activities of abductor hallucis and adductor hallucis between the short foot and toe-spread-out exercises in subjects with mild hallux valgus

J Back Musculoskelet Rehabil. 2013;26(2):163-8. doi: 10.3233/BMR-2012-00363.

Gait and any form of locomotion are highly complicated with many pieces necessary to achieve clean, smooth, coordinated motion.
Failure in only one piece of the puzzle can result in profound unhinging of the entire system because of the entangled nature of the feedback loops.
“ Proprioceptive feedback from extensor muscles during the stance phase ensures that the leg does not go into swing when loaded and that the magnitude of extensor activity is adequate for support. Proprioceptive feedback from flexor muscles towards the end of the stance phase facilitates the initiation of the swing phase of walking. Evidence that muscle afferent feedback also contributes to the magnitude and duration of flexor activity during the swing phase has been demonstrated recently. The regulation of the magnitude and duration of extensor and flexor activity during locomotion is mediated by monosynaptic, disynaptic, and polysynaptic muscle afferent pathways in the spinal cord. In addition to allowing for rapid adaptation in motor output during walking, afferent feedback from muscle proprioceptors is also involved in longer-term adaptations in response to changes in the biomechanical or neuromuscular properties of the walking system.” - Lam and Pearson
Neuroscientist. 2004 Jun;10(3):247-59. Cerebellar control of balance and locomotion. Morton SM1, Bastian AJ.

What ischial-femoral impingement might look like as aberrant shoe wear.

A few weeks ago we wrote an article on ischial-femoral impingement. For you to best understand today’s blog post you really should go back and review this interesting clinical phenomenon, here is the link to that piece.

Three weeks ago a talented marathoner came into our office complaining of a long standing deep posterior right hip pain and an equally longstanding left chronic lateral ankle and foot pain.  The ankle had been treated regularly for chronic peroneal tendonitis with various manual therapy modalities and yet the right hip seems to be left out of the equation in terms of treatment.

After taking a detailed history this runner unknowingly pretty much told us they had all the qualifications of ischial-femoral impingement (IFI).  What they did not realize was that they had a cross over gait style that was a significant contributor to the clinical problem.  

Lets now have a look at the shoe wear patterns above. On the left shoe, (a shoe we love, New Balance Fresh Foam (find your next pair at NewBalance Chicago)) we see that the entry zone or crash zone of rear foot impact is heavily worn, especially laterally. Heavy entry zone wear can be from several things, but one thing we always check for and assume until proven otherwise is a cross over gait. It can also just be from excessive rearfoot inversion at foot strike but when excessive there is usually a reason for it, especially when unilaterally as seen here. This foot is not stacking under the knee and hip, it is striking more midline to a plumb line dropped from the hip joint. This creates a steep medial angle of attack. The question is why ? Well, in the history the right hip pain began first and then the left ankle pain, so one should at least consider a compensatory timeline, that being the foot is a compensation in the gait cycle from the painful hip.

This client on examination tested pretty obviously for a right frontal plane drift, meaning when the right foot impacts there is not enough lateral line support to hold the hip/pelvis over the foot and so the pelvis drifts laterally to the right in this case. This can be fought by inverting the foot. This is a strategy to try and stop the lateral drift.  In this case, excessive wear is seen on the entire lateral side of the right shoe to represent this compensation. Changing this clients foot wear, shoe, orthotic is not fixing the problem, in fact it is impairing their ability to compensate and could create more problems, and even another deeper layer of compensation. Again, the inverted/supinated right foot moves the weightbearing line laterally, by moving the foot’s center of pressure from within the confines of the foot tripod towards the lateral border of the foot tripod, in attempt to restack the loading over the laterally drifted hip (hence the right lateral shoe wear pattern). Unfortunately this does not solve the reason for the lateral drifted pelvis. That solution has to come from improved stablization of the hip, pelvis and core and since they tested weak on the right side abdominals, gluteus medius, gluteus max and other  accessory lateral stabilizers,  work must be done there. Interestingly, this runner is stuck into a vicious cycle. The lateral drift to the right is allowing the left hemi-pelvis to dip and this is challenging rotational control of the stance limb and it is causing ischial-femoral impingement (suspecting of the quadratus femoris).  It was clear on examination that there was impairment of the quadratus femoris and obturator externus upon detailed testing and deep palpation was pin point tender over these structures.  Resistance to rotational challenges to the limb, especially iso and eccentric internal rotational challenges, were very poor when it came to coordination, endurance and certainly strength.

Remember, when you are spending time going sideways (right frontal plane drift), you are not spending time moving forwards. This could cause an early right departure and force and early left stance engagement.  But it goes deeper than that in this case.  Here, the right frontally drifting pelvis will pull the left swing leg across the midline with it, creating a left cross over gait.  This will make more sense if you watch our popular video here. Link

So, when this left swing leg is forced into the cross over gait variant, it will force a strong lateral heel strike, as evidenced on the left shoe wear. This is a compensation to what is going on in the right side body mechanics.

Can a cross over occur on one side of the body ? Sure, this case is a perfect example.

Can a cross over gait on the left in this case, cause a vicious cycle and in itself create an environment whereby a right ischio-femoral impingment occurs ?  Sure, neuronal plasticity can be a bitch, it can work in your favor, and against you.

This is not a tough case, if you have seen the beast before and you recognize all of its parameters. If you have not seen the beast before, this case is a nightmare with all these pieces (deep buttock pain, impingement, frontal drift, cross over, strange shoe wear pattern, opposite ankle peroneal pain etc).  Do you have to get this right every time with a bulls eye diagnosis and remedy? Heck no, we flounder every day with new things and variants of old. Sometimes the layers of compensations are so deep that it takes weeks before a recognizable layer presents itself. Patience on both the client and the doctor are necessary.  

So what we have here is a fairly classic shoe wear pattern of a right laterally drifting pelvis and a cross over left leg. In this case it was from a weak right core and pelvis drift creating an environment for the generation of a right ischial-femoral impingement syndrome, driving a left peroneal tendonopathy scenario from the ensuing left cross over gait.  

Remember, don’t fix your clients shoe wear pattern and certainly do not make shoe recommendations from what you see in their shoe wear pattern. Recommending a different shoe to fix this clients problem is a mistake. As is prescribing an orthotic, different foot bed, adding wedges and postings to the shoe or foot bed can also be  mistake. Define the source of the problem, before you go start tinkering around with the bottom of the kinetic chain. Want more ? Try taking our National Shoe fit program to get deeper into this kind of stuff.

We were lucky enough to get this runner’s problem spot on. After many failed attempts by others, this case was 50-75% resolved in one session with the right homework and a great understanding by the runner of their problem. They fully engaged themselves in the understanding of the problem and what they needed to be aware of in their walking and running gait. They were diligent with their homework and understood how it would help the presentation. They presented again to the clinic this week for a focused session to drive the problem further out of town and they are now on their way to the Boston Marathon with a smile and tools to fix the problem. There is a little more fine tuning to do here, but we can wait until they return from Boston.

Good luck in Boston everyone !

We hope this case helps you help someone else, that is the point after all.

Shawn and Ivo, the gait guys

The Serratus and Gait..

Think about the role of the serratus anterior in gait. Now think about it in martial arts. There are profound neuromuscular and fascial connections and implications here. Just like the thoracolumbar fascia which also attaches to the ribs, these muscles seem to be necessary for core stability.

“Conclusions: Simultaneous recruitment of the lower extremity and trunk muscles increases the activation of the SA
muscle during the FPP exercise.
Clinical Relevance: Rehabilitation clinicians should have understanding of the kinetic chain relationships between
the LE, the trunk, and the upper extremity while prescribing exercises. The results of this study may improve clinicians’
ability to integrate the kinetic chain model in a shoulder rehabilitation program. ”

The authors also suggest a hierarchy of exercise to follow. An interesting read for a Sunday.

great full .pdf here: http://www.ncbi.nlm.nih.gov/…/PMC42751…/pdf/ijspt-12-924.pdf

How well do you understand stance phase mechanics?

Here is a recent question we fielded and thought it would make a great post. 

Question/Comment: I’m slightly confused about closed chain hip motion in the stance leg.

Maybe if I explain what my thought process is you can correct me.  Lets use
left stance phase with the right leg swinging through.

After right mid-swing, the pelvis will be rotating towards the left.  The
motion of the pelvis on the left femur would be relative femur internal
rotation.  I understand that the right leg is externally rotating
(supinating) and that normal open chain kinematics of hip extension is
coupled with external rotation.  But if the pelvis is moving towards the
left AND the left femur externally rotates, wouldn’t that create too much
rotation?  So what I’m saying is that a pelvis that is oriented to the left
with a left femur that externally rotates creates an odd motion in my head
(which may be where the problem lies).  If you’ve ever seen a western where
the gun slingers do that weird walk to a shoot out…that’s what an
externally rotating femur during terminal stance looks like to me.

I’ve discussed this with other clinicians.  Some are in agreement with me,
some think it’s externally rotating, and some don’t know what I’m talking
about.  In my patients I also see a loss of hip IR more than hip ER.  These
patients that lose hip IR seem to have more difficulty in terminal
stance/toe-off phase more than the ones that lose hip ER.

If you could help me understand these kinematics and clear this up for me I
would greatly appreciate it.

Thank you, A

our reply: 

Taking your example with the L leg in stance:
When the L heel contacts the ground, the friction of the ground (hopefully) slow the calcaneus and the talus slide anteriorly on the calcaneus. 

Because of the shape of the calcaneal facets, the talus plantar flexes, adducts and everts. This sets the stage for pronation to occur: the calcaneus everts and the lower leg internally rotates, with the thigh following. The right side of the pelvis is moving to the L (counter clockwise rotation). This should occur (ideally) until midstance. At midstance, the opposite ® foot begins to enter swing phase; this should initiate supination of the stance phase leg (L). At this point, the L foot should be beginning to supinate the the leg and thigh beginning external rotation. It (thigh and leg) should reach maximal external rotation at toe off (maximal counter clockwise rotation of the pelvis) and remain in external rotation until heel strike/initial contact on the L side again. At this point, the pelvis begins clockwise rotation.

It is necessary for the thigh and leg to externally rotate while the pelvis is rotating counter clockwise, because of the constraints of the iliofemoral, pubeofemoral and ishiofemoal ligaments.

We too often see a loss of internal rotation of the hip in symptomatic populations more often than external rotation.

We hope this clarifies things for you.

Thank you again for the question and taking the time to write.

The Gait Guys

The deeper your knowledge and experiences, the more things you will see. As in life, the more experiences you have the wiser you become and the clearer the bigger picture becomes. All these things enrich the experience or observation. These experiences take simple black and white and render an infinite palate of grey tones. 

To the untrained observer, these are just two feet. With a little more experience these are two feet of different length. Deeper further, these are two different sized feet with different plantar pressure responses (helped here by increasing the greyscale contrast). Deeper yet, this represents a left foot (viewers right) that has a dysfunctional flexor digitorum longus (FDL) and lateral quadratus plantae muscle. All of these observations allow the skilled and knowledgeable viewer to extrapolate and theorize, with clear thought processes, which leg could be shorter/longer, how the pelvis might be distortioned, step length and stride length variability, foot stability and so much more.

The life long student does not need the contrast enhanced picture on the right to heighten the visibility of the plantar pressures, but it helps.  This is what wisdom and experience do, they enable you to look deeper into something and to see it for what it truly is, not what it appears to be.

Come listen to our teleseminar tonight (Wednesday March 18th, 2015) on www.onlinece.com at 7pm central. Log in early to get set up. Come listen in while we delve into one of the bigger questions, if the left foot (viewers right) is longer it has likely pronated more over a longer period of time stretching out plantar soft tissues and corrupting joint function in multiple areas. But if this is the case, why then are they presenting with plantar pressures that are more representative of supination standards ?  

This is mental gymnastics. It is good stuff to do regularly, even though this is a static presentation, many good theories and thoughts can be brought forth. Getting the answer is not the goal, getting the thought process down is.

The more you know, the more truth you will see.

See you tonight, we will break this down into a microscopic level that will challenge you all.

Shawn and Ivo, the gait guys

The all to common case of the Wobbling Hexapod (Tripod) : Is Your Foot hexa/Tripod Stable Enough to Walk or Run without Injury or Problem ?

Note the music we have chosen today. We tried to match the rate of the dancing tibialis anterior tendon to the tempo of the song, just for fun of course. Well, actually, for neurological reasons as well, as with a steady tempo or beat, your nervous system can learn better. Why do you think we teach kids songs to learn (or you can’t get the theme from the “Jetsons” out of your head).

This is a great video. This client has an obvious problem stabilizing the foot tripod during single leg stance as seen here.  There is also evidence of long term tripod problems by the degree of redness and size (although difficult to see on this plane of view) of the medial metatarsophalangeal (MTP) joint (the MPJ or big knuckle joint) just proximal to the big toe.  This is the area of the METatarsal head, the medial aspect of the foot tripod.

As this client moves slowly from stance into a mild single leg squat knee bend the challenges to the foot’s stability, the tripod, become obvious.  Stability is under duress. There is much frontal plane “Checking” or shifting and the tibial and body mass is rocking back and forth on a microscopic level as evidenced by the dancing tibialis tendon at the ankle level.  The medial foot tripod is loading and unloading multiple times a second. 

Is it any shock to you that this person has chronic foot problems which are exacerbated by running ?  Every time this foot hits the ground the foot is trying to find stability. The medial tripod fails and the big knuckle joint (the 1st MPJ or big toe joint) is enlarging from inflammation, uncontrolled loading through the joint, and early cartilage wear and decay, not to mention the knee falling medially to the foot line as well.  Hallux limitus (turf toe) is subclinical at this time, but it is on the menu for a later date. A dorsal crown of osteophytes (the turf toe ridge on the top of the foot) is developing steadily, soon to block out the range necessary for adequate toe off in this client.  And that means a limitation in  hip extension sometime down the road (and premature heel rise……. did you read Wednesday’s blog post on that topic ?).

*addendum:

Take the time to develop the skill. We ask our clients to work on standing with the toes up to find a clean tripod and do some shallow squats working on holding the tripod quietly. Be sure your glutes are in charge, spin of the limb is in part controlled at the core-hip level so that can a primary location to hunt as well. Eventually work into toes pressed flat but be sure the tripod is still valid, esp the medial tripod. Don’t be what Dr. Allen refers to as a “knuckle popper”. No toe curling/hammering either. Keep that glute on. Move the swing leg forward during a lunge, and then behind you during a squat (mimicking early and late midstance phases of gait/running). This will help your brain realize when it needs this stability and it will also act to press you off balance and will make the foot check and challenge. Do this until you feel the foot fatigue on the bottom. Then Stop. Repeat later. If the medial tripod collapses, the knee will drop inwards and excess pronation is inevitable. We modified this with our prescription of the “100 ups”…..combine the two !

Shawn and Ivo … .  comfortably numb.

Once you have been to the Dark Side of the Moon  (and hopefully you didn’t have any Brain Damage) you will know it well and know what to expect when you return again.  Meaning, when you have seen these issues over and over again, hopefully in your daily work if not regularly here at The Gait Guys, you will quickly know what things to assess and look for in your athletes.  And you might just turn into a Pink Floyd fan at the same time, or at least crave some Figgy Pudding (but you have to eat yer’ meat! How can you have any pudding if you don’t eat  yer’ meat?).

I have been playing with some of this guys work. \
Like respect, flexibility is earned. It is earned through the proper strength, on fundamentally clean motor patterns. Flexibility without strength is not all that common. But we spend so much time stretching and forcing length, and this is a flawed path that will not get you far or to places you truly want to be.  There are many methods, but slow clean movements are important in the early stages, just like in this video. I like to use the 9 second rule in most reteaching in my clinic, 4 seconds to get to the desired end movement, 1 second to hold the end skill, and 4 seconds to get back out of the skill.  Modify as you like and as necessary. Speed can cheat.  Remember, skill first, then endurance and repeatability on the skill, then strength on the endurance based skill.  S.E.S !
This is a Beautiful video, beautiful movements, amazing strength and flexibility.  Things to strive for (and it can’t hurt my Jiu Jitsu either :)  -Dr. Allen

The partial truth about the Foot Tripod. The HEXApod.

The gait guys have talked about the foot tripod for a very long time. But the truth of the matter is that it is really a HEXApod. HEXA means 6. And when the foot is properly orientated and engaged on the ground, the 5 metatarsal heads and the heel should all be engaged with the ground, truly making it an asymmetrical hexapod. In an ideal scenario, the foot would be most stable if it looked like the strange symmetrical hexapod above with the contact points equally distributed around a center point. But that is not the human foot and this version of a hexapod is far simpler and likely inferior to the foot hexapod when human locomotion is to be attempted. The human foot is engineering marvel when it works properly.  

Perhaps the best example of what I mean by the foot being a HEXApod is in the pressure diagram above. In that first picture, on the right of that picture, we see multiple pressure points under the metatarsal heads of the right foot.  Minus the missing 1st metatarsal head pressure point (taken over by increased flexor hallucis longus activity represented by increased pressure at the big toe),  this pretty much confirms that the foot is not a tripod, rather a hexapod. The theory of the tripod, the 1st and 5th metatarsal heads and the heel, is only crudely accurate and honest. In this picture case, this person has increased lateral foot weight bearing (possibly why the 1st MET head pressure is absent) and possibly represented by pressure under the base of the 5 metatarsal. This is not normal for most people and if this person could get the 1st MET head down, they might even have a HEPTApod foot structure because of the 5th metatarsal base presentation (which sometimes represents peroneal muscle weakness). 

Where did we lead you astray after all these years of “tripod” talk ? We have always discussed the foot tripod. We have always discussed the imperative need to keep the limb’s plumb line forces within the area represented by the tripod.  If your forces fall more laterally within the tripod, as in this first discussed picture, one is at increased risk of inversion events and the myriad of compensations within the entire body that will occur to prevent that inversion. So again, why the tripod?  Well, it is easier to understand and it serves our clients well when it comes to finding active foot arch restoration as seen in this video of ours here.  But, the truth of the matter is that all of the metatarsal heads should be on the ground. The 2nd METatarsal is longer, the 3rd a little shorter, and the 4th and 5th even a little short than those. With the 1st MET shorter, these 5 form a kind of parabolic arc if you will. Each metatarsal head still should contact the ground and then each of those metatarsals should be further supported/anchored by their digits (toes) distally.  So the foot is actually more truly a HEXAPOD. Take the old TRIPOD theory we have always spoken about and extend a curved line beyond the forefoot bipod points (1st and 5th metatarsals) to incorporate contact points on the 2, 3 and 4th metatarsal heads. These metatarsals help to form the TRANSVERSE arch of the foot. It is this transverse arch that has given us the easily explainable foot TRIPOD because if a line is drawn between just the shorter 1st and 5th metatarsals, we do not see contact of the 2-4 metatarsal heads when we only look for pressure between these two bipod landmarks, but the obvious truth is that the 2-4 metatarsals are just longer and extend to the ground further out beyond this theoretical line drawn between the 1st and 5th MET heads.   

So, the foot is a HEXAPOD. Make no mistake about it. It is more stable than a tripod because there are more contact points inside the traditionally discussed foot tripod model. And frankly, the tripod theory is just a lie and just too fundamentally simple, unless you are an American 3 toed woodpecker.

Dr. Shawn Allen,     www.doctorallen.co

one of the gait guys

Some stuff you need to know about running spikes.

I see many track runners in my office, from middle school all the way into the USA Masters Division.  A few years ago one of the top USA Masters Milers came to see me on Friday before heading off to a national meet. He showed me some of his spikes (see pics above) and complained the there was something off on the spikes on the left, the Nike Mambas.  The shoe to the right is the Nike Zoom Miler.

You need to understand a bit of the physics of running turns to understand what is missing for this runner in this pair of spikes.  Things do change if you are running on a sloped track, but those are only found indoors and are not all that common to run on for most folks so we will stick with the thinking on flat tracks.

What you should be able to easily detect is that the Nike Mamba’s are missing the lateral 5th metatarsal forefoot spike on the cleat plate.  And you need to then realize that this is the right shoe, so it is the outside foot/leg on the track. It is the foot that will be pushing off harder from the outside on the turns to keep the centripetal forces of running a curve from allowing the runner to fall off the curve into the outer lanes. This right foot will always be pushing from outside to inside to maintain the body’s progression in the desired lane, when running the curves.

Think about it for a minute. In order to run in a circle, or a curve in this situation, the outside foot always has the tendancy to be more inverted to keep foot contact on the ground. This is where a Forefoot varus MIGHT come in handy ! This means the foot will be tipped to the outside a little, because of the curve and because the body will be leaning into the center of the track on the curves. Thus the foot and shoe will be relying on more lateral foot pressures to drive the body mass back into the lane since centripetal forces will always be driving you laterally out of the lane.  Thus, the lateral spikes on the right foot must be accommodating.  In the case of the Mamba shoe. there is only a sheet of black hard plastic over the midshaft-head of the 5th Metatarsal on the lateral foot. It is no wonder the runner was feeling like he was slipping on the turns (the front of the midfoot was not anchored to the ground, only the forefoot due to the spikes in that location). You can see clear evidence of the lateral slipping in the picture. Can you see the orange/brown patch where he was slipping ? A spike there in that area would have been wonderful.  Slipping is a power leak and a risk for injury.  If the foot is trying to gain purchase into/onto the track with the foot inverted there needs to be traction at that lateral foot, what is referred to as the Lateral Column.  You can see why the Nike Zoom Miler was a better choice, there is a nice spike placement under the lateral foot for just this measure, and there is no evidence of slippage wear.  He told me that the Mamba was a steeplechase designed shoe but we still both felt that the issue remained relevant even in that event. The Nike website however states that “the Nike Zoom Mamba Men’s Track and Field Shoe is perfect for the 800-5000m track athlete” so we think they have missed an issue here in our opinion.

I could make a better case for the Mambas if  they were for a 100m straight run but I would still like a 5th metatarsal /lateral spike where there isn’t one.  I will occasionally file spikes to get the perfect feel for the athlete.  It is usually the 5th metatarsal and 1st metatarsal spikes I mess with, merely to help hone the athletes feel on the track. The problem is that each track has a different feel so it is less of an occurrence in recent years.

It is good to know your shoes, it is good to know your physics. It is great to know them both and melt them together to solve problems.  Not all spikes are created equal, not all tracks are the same, not all events are the same and certainly not all feet and the athlete’s who own them are the same.  And on the topic of Forefoot Foot types, both the forefoot varus and forefoot valgus foot might have a problem with the Mamba’s depending on their strength, skill and strategies for ground purchase.  Hopefully your shoe store and your track and cross country coaches know these issues. You might want to bring this blog post to their attention however, just in case.

Dr. Shawn Allen

Tom Purvis hits some strong points in this video about squatting, hip hinges, ankle dorsiflexion, and movement as a whole.  * Keep in mind, this is all sagittal plane stuff….. it gets far more complicated when there are lateral (frontal) plane or rotational (axial) considerations ….. these are the “knees out” dialogues and debates you have read over and over on the web in the last year.

Dr. Shawn Allen

addendum:

Food for thought after posting today’s Tom Purvis squat video.

Could this study below translate into the statement/question: 

“attempting to achieve sufficient dorsiflexion through the combined ‘foot pronation-ankle dorsiflexion’ mechanism, as opposed to just dorsiflexion from the ankle mortise joint alone, may change the dynamics of the entire limb…. in this case, hip flexion range observation. Is this because when dorsiflexion is cheated via foot pronation, instead of just ankle dorsiflexion, there is more internal tibia/femoral spin than would normally occur from just sagittal ankle hinging which can in turn impair terminal hip flexion range via impingement type action ? I think so. It would be cool to see what would have happened in the study had the pronating clients been shown my foot tripod restoration exercise (it’s on youtube).   -Dr. Allen

here is some new research on this point, for what it is worth.  It keeps the mind thinking though.

J Phys Ther Sci.  2015 Jan;27(1):285-7. doi: 10.1589/jpts.27.285. Epub 2015 Jan 9.The kinematics of the lower leg in the sagittal plane during downward squatting in persons with pronated feet.  Lee,Koh da,  Kim 

Abstract

[Purpose] This study aimed to examine changes in lower extremity kinematics in the sagittal plane during downward squatting by subjects with pronated feet. [Subjects and Methods] This study selected 10 subjects each with normal and pronated feet using a navicular drop test. The subjects performed downward squatting, in which the knee joints flex 90° in a standing position. We recorded the angles of the hip, knee, and ankle joint in the sagittal plane through motion analysis. For the analysis, the squatting phase was divided into phase 1 (initial squat), phase 2 (middle squat), and phase 3 (terminal squat) according to the timing of downward squatting. [Results] In the pronated foot group comparison with the normal group, thehip joint flexion angle decreased significantly in phases 2 and 3. The dorsiflexion angle of the ankle joint increased significantly in phase 3. The flexion angle of the knee joint did not differ between groups in any of the phases. [Conclusion] The pronated foot group utilized a different squat movement strategy from that of the normal foot group in the sagittal plane.

Rewiring.

The peripheral and central nervous systems are functionally
integrated regarding the consequences of a nerve injury: a
peripheral nerve lesion always results in profound and long lasting
central modifications and reorganization. (Kaas, 1991)
Does there need to be a lesion though ? A functional lesion will force changes just like an ablative lesion. Altered gait that persists from a sprained ankle or a painful knee will force central modifications and reorganization. This is why resolution of pain and aberrant function is critical. If you rehab to 80% you leave 20% on the table and that gets rewired into the system as the new norm. Remember, the entire system is watching, learning, adapting and rewiring all the time. This is why you must have a team in place to resolve all, if possible, of your client’s deficits. If you leave 20% of a problem on the table, and add endurance and strength to the “80%resolved:20%remaining”, you reorganize the central nervous system with that as the assumed norm moving forward. From this point forward, this is the architecture that all new patterns and forms are built from.  This sets up for long term rewiring of all of the connected parts, from motor, sensory, visual, gait, proprioceptive, vestibular and the list goes on and on. If you have ever wondered how a client can have so many areas of pain and dysfunction you might want to go back into their history and ask them if there was a single injury or event that occurred after which all their new problems started to stack up. 

If you are a gait analysis junkie, remember this principle above. All of the things you see in a person’s gait are not unconnected in many cases.  Much of what you see is a compensation around their problems, not the actual problem. 

Remember this principle: the peripheral nervous system attempts to repair by regrowth, the central nervous system attempts to repair by re-routing and reorganizing.

Dr. Shawn Allen

Our neurology mentor, Dr. Carrick discusses the vestibular system and what can go wrong with it and what happens to our locomotion system when it doesn’t function properly.  

Know this gait, memorize it.  It is NOT a Parkinsonian gait. 

Here is what you need to know about the gait presentation in Normopressure hydrocephalus (NPH):

The gait changes are often subtle and progress as NPH progresses because of the changes in the brains ventricular tissues eventually compromising the sensory-motor tracts.
Early gait changes, MILD, may show a cautious gait. Steps length and stride length may be slowed and shortened. The gait may begin to show signs of being deliberate and calculated, less fluid and free. The appearance of unsteadiness or balance challenges may prevail. Once simple environmental obstacles may now present as challenges, things like curbs, stairs, weaving between tables in restaurants or wide open spaces where there is nothing to grasp onto for stability. Weakness and tiredness of the legs may also be part of the complaint, although examination discloses no paresis or ataxia. (Ropper)  A walking aid such as a cane may add comfort but often appears to be rarely used.

As the gait changes progress into the more MODERATE to ADVANCED, the walking aids used often progress into quad walkers.  Wheelchairs are needed in more difficult places or when fatigue is growing factor.  As the gait challenges progress, the careful observer will note a more obvious reduction in step and stride length, a head down posture, less dual tasking engagement during gait execution, slowed walking speed, reduced foot-floor clearance, shuffling gait (keeping the feet more engaged to the ground, this can be a Parkinsonian-type gait mis-read, there will be no tremor or rigidity), searches for stable external cues (reaching for railings, a kind arm or hand, touching walls etc), widening of the feet (broad based stance), and fears of falling backward.

In the most ADVANCED gait impairments, the fear of falling can become too great. There may even be an inability to engage sit-stand-walk motor patterns and the fatigue of the limbs may be too advanced to even stand let along walk. This stage is referred to as Hydrocephalic astasia-abasia (Ropper).  

Normopressure Hydrocephalus is a serious issue if left unrecognized and untreated.  NPH must be diagnosed early on since a delay in reducing the pressure on the cortical tissues can lead to permanency of disease and dysfunction.  According to Poca there can be a wide range of successes and failures in symptom remediation, but there is clearly a time dependency on early diagnosis. Thus, clearly recognizing any early gait changes and behaviors prior to advancing incontinence and mental decline is paramount.

Dr. Shawn Allen, … one of “the gait guys”

Some of the above was inspired and summarized by this great article, from the Boston Globe.  

References:

1. Marmarou, Anthony; Young, Harold F.; Aygok, Gunes A. (1 April 2007). “Estimated incidence of normal-pressure hydrocephalus and shunt outcome in patients residing in assisted-living and extended-care facilities”. Neurosurgical FOCUS 22 (4): 1–8.

2. Ropper, A.H. & Samuels, M.A. (2009). Adams and Victor’s Principles of Neurology (9th edition). New York, NY: McGraw-Hill Medical.

3. Poca, Maria A.; Mataró, Maria; Matarín, Maria Del Mar; Arikan, Fuat; Junqué, Carmen; Sahuquillo, Juan (1 May 2004). “Is the placement of shunts in patients with idiopathic normal pressure hydrocephalus worth the risk? Results of a study based on continuous monitoring of intracranial pressure”. Journal of Neurosurgery 100 (5): 855–866.

4. Am J Phys Med Rehabil. 2008 Jan;87(1):39-45.
Objective assessment of gait in normal-pressure hydrocephalus.
Williams MA1, Thomas G, de Lateur B, Imteyaz H, Rose JG, Shore WS, Kharkar S, Rigamonti D.

5. Clin Neurophysiol. 2000 Sep;111(9):1678-86.
Gait analysis in idiopathic normal pressure hydrocephalus—which parameters respond to the CSF tap test?
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Diercks C, Palmié S, Mehdorn HM, Illert M, Deuschl G.

6.Rev Neurol (Paris). 2001 Nov;157(11 Pt 1):1416-9.
[Postural and locomotor evaluation of normal pressure hydrocephalus: a case report]. Mesure S1, Donnet A, Azulay JP, Pouget J, Grisoli F.

7.J Neurol Neurosurg Psychiatry. 2001 Mar;70(3):289-97.
Comparative analysis of the gait disorder of normal pressure hydrocephalus and Parkinson’s disease.
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Illert M, Deuschl G.

#normopressure hydrocephalus

#NPH

#gait problems

#balance

#incontinence

#dementia

#parkinsons

#parkinsons disease

#falls

#balance problems

#alzheimers

“If the software in your brain does not acknowledge the change in hardware – the better moving joint, the more elastic muscle, the better firing pattern between your stabilizers and prime movers – it does not matter.” - Gray Cook

We could not agree more. No matter how much table work you do or how much rehab you do, if you do not teach your client how to use the changes in walking, running, locomotion through specific retraining, then the changes are useless. Newly acquired skills that are not made accessible to meaningful locomotion were a waste of time.

A Wobble in the System: The Gait Changes in Normopressure Hydrocephalus

Can you afford to miss this diagnosis ? 

Today, the gait changes in NPH are discussed because as with many neurologic disorders and diseases, subtle gait changes are the first signs. And, in this disorder, you have to catch the gait changes early on in order to give your client the greatest changes of full recovery.   Today we couple this blog post with a great video story of a missed case study of NPH.

Normopressure hydrocephalus (NPH) consists of the triad of :

1. gait disturbance
2. urinary incontinence
3. dementia or mental decline

In the most general terms, Normal pressure hydrocephalus (NPH), also referred to as symptomatic hydrocephalus, is caused by a decreased absorption of cerebrospinal fluid (CSF). The resultant increased intracranial pressure can cause ventriculomegaly.  In NPH patients, the pressure remains just slightly elevated, but enough to create pressure on the cortical tissues of the brain causing the symptoms above. The vagueness of this problem and its seemingly random symptoms is primarily why this disorder is often missed or misdiagnosed as dementia, Parkinson’s or Alzheimers disorders.

As discussed previously, many early neurological diseases and disorders softly present with early gait changes. And, as in NPH, gait changes may be the earliest symptom of the 3 mentioned earlier. One’s ability to know, observe and recognize abnormal gait patterns coupled with a good historical interview and physical exam can often tease out the earliest manifestation of NPH.

Here is what you need to know about the gait presentation in NPH:

The gait changes are often subtle and progress as NPH progresses because of the changes in the brains ventricular tissues eventually compromising the sensory-motor tracts.
Early gait changes, MILD, may show a cautious gait. Steps length and stride length may be slowed and shortened. The gait may begin to show signs of being deliberate and calculated, less fluid and free. The appearance of unsteadiness or balance challenges may prevail. Once simple environmental obstacles may now present as challenges, things like curbs, stairs, weaving between tables in restaurants or wide open spaces where there is nothing to grasp onto for stability. Weakness and tiredness of the legs may also be part of the complaint, although examination discloses no paresis or ataxia. (Ropper)  A walking aid such as a cane may add comfort but often appears to be rarely used.

As the gait changes progress into the more MODERATE to ADVANCED, the walking aids used often progress into quad walkers.  Wheelchairs are needed in more difficult places or when fatigue is growing factor.  As the gait challenges progress, the careful observer will note a more obvious reduction in step and stride length, a head down posture, less dual tasking engagement during gait execution, slowed walking speed, reduced foot-floor clearance, shuffling gait (keeping the feet more engaged to the ground, this can be a Parkinsonian-type gait mis-read, there will be no tremor or rigidity), searches for stable external cues (reaching for railings, a kind arm or hand, touching walls etc), widening of the feet (broad based stance), and fears of falling backward.

In the most ADVANCED gait impairments, the fear of falling can become too great. There may even be an inability to engage sit-stand-walk motor patterns and the fatigue of the limbs may be too advanced to even stand let along walk. This stage is referred to as Hydrocephalic astasia-abasia (Ropper).  

Normopressure Hydrocephalus is a serious issue if left unrecognized and untreated. Here is yet another reason why you must be familiar with this problem:

“Patients with dementia who are confined to a nursing home and may have undiagnosed NPH can possibly become independent again once treated. So far only one study was able to evaluate the prevalence of NPH, both diagnosed and undiagnosed, among residents of assisted-living facilities, showing a prevalence in 9 to 14% of the residents.” - Marmarou

One’s lack of awareness and knowledge, are one’s greatest enemies. If you don’t know something exists, because you’ve never studied or learned it, how can you be aware of it ? If you’re not spending enough time examining a client, you might be unaware of an issue even though you may be knowledgeable about the issue. One must have both awareness and knowledge. One must also be aware that compensations are the way of the body. What you see is not your client’s problem. It is their strategy to cope.

NPH must be diagnosed early on since a delay in reducing the pressure on the cortical tissues can lead to permanency of disease and dysfunction.  According to Poca there can be a wide range of successes and failures in symptom remediation, but there is clearly a time dependency on early diagnosis. Thus, clearly recognizing any early gait changes and behaviors prior to advancing incontinence and mental decline is paramount.

Bonus: here is a little bonus tidbit for my fellow neuro gait friends. 

Stolze (7) study conclusion: “The gait pattern in normal pressure hydrocephalus is clearly distinguishable from the gait of Parkinson’s disease. As well as the basal ganglia output connections, other pathways and structures most likely in the frontal lobes are responsible for the gait pattern and especially the disturbed dynamic equilibrium in normal pressure hydrocephalus. Hypokinesia and its responsiveness to external cues in both diseases are assumed to be an expression of a disturbed motor planning.”

Dr. Shawn Allen, … one of “the gait guys”

Some of the above was inspired and summarized by this great article, from the Boston Globe.  

References:

1. Marmarou, Anthony; Young, Harold F.; Aygok, Gunes A. (1 April 2007). “Estimated incidence of normal-pressure hydrocephalus and shunt outcome in patients residing in assisted-living and extended-care facilities”. Neurosurgical FOCUS 22 (4): 1–8.

2. Ropper, A.H. & Samuels, M.A. (2009). Adams and Victor’s Principles of Neurology (9th edition). New York, NY: McGraw-Hill Medical.

3. Poca, Maria A.; Mataró, Maria; Matarín, Maria Del Mar; Arikan, Fuat; Junqué, Carmen; Sahuquillo, Juan (1 May 2004). “Is the placement of shunts in patients with idiopathic normal pressure hydrocephalus worth the risk? Results of a study based on continuous monitoring of intracranial pressure”. Journal of Neurosurgery 100 (5): 855–866.

4. Am J Phys Med Rehabil. 2008 Jan;87(1):39-45.
Objective assessment of gait in normal-pressure hydrocephalus.
Williams MA1, Thomas G, de Lateur B, Imteyaz H, Rose JG, Shore WS, Kharkar S, Rigamonti D.

5. Clin Neurophysiol. 2000 Sep;111(9):1678-86.
Gait analysis in idiopathic normal pressure hydrocephalus–which parameters respond to the CSF tap test?
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Diercks C, Palmié S, Mehdorn HM, Illert M, Deuschl G.

6.Rev Neurol (Paris). 2001 Nov;157(11 Pt 1):1416-9.
[Postural and locomotor evaluation of normal pressure hydrocephalus: a case report]. Mesure S1, Donnet A, Azulay JP, Pouget J, Grisoli F.

7.J Neurol Neurosurg Psychiatry. 2001 Mar;70(3):289-97.
Comparative analysis of the gait disorder of normal pressure hydrocephalus and Parkinson’s disease.
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Illert M, Deuschl G.

Rearfoot to Hip Pathomechanical considerations.

In normal gait, the rearfoot strikes in slight inversion and then quickly moves through eversion in the frontal plane to help with the midfoot through forefoot pronation phases of gait. Some sources would refer this rearfoot eversion as the rearfoot pronatory phase, after all. pronation can occur at the rear, mid or forefoot. As with all pronation in all areas, when it occurs too fast, too soon or too much, it can be a problem and rearfoot eversion is no different.  If uncontrolled via muscles such as through tibialis posterior eccentric capabilities (Skill, endurance, strength) or from a structural presentation of Rearfoot Valgus pain can arise. 

From a scenario like in the video above, where a more rearfoot varus presentation is observed,  where the lateral to medial pronation progression is excessive and extreme in terms of speed, duration and magnitude this can also create too much lateral to medial foot, ankle and knee movement.  This will often accompany unchecked movements of internal spin through the hip. So one should see that these pronation and spin issues can occur and be controlled from the bottom or from the top, and hopefully adequately from both in a normal scenario.  It is when there is a biomechanical limitation or insufficiency somewhere in the chain that problems can arise. And remember, pain does not have to occur where the failure occurs, in fact it usually does not. So when you have knee pain from an apparent valgus posturing knee, make sure you look above and below that knee.  Also, keep in mind that as discussed last week in the blog post on ischiofemoral impingment syndrome (link), these spin scenarios can be quite frequently found with ipsilateral frontal plane lateral deviations (bumping of the hip-pelvis outside the vertical stacking of the foot-knee-hip stacking line). This stacking failure can also be the source of many of the issues discussed above, so be sure you are looking locally and globally. And remember, what you see is not the problem, it is their compensation around their deeper problem quite often.

If you have not read the blog post from last week on ischiofemoral impingement syndrome you might not know where the components of the cross over gait come in to play here nor how a rearfoot problem can present with a hip impingement scenario, so I can recommend that article one more time.

One last thing, just in case you think this stuff is easy to work through, remember that these rearfoot varus and valgus problems, and pronation rates. and limb spin rates are all highly variable when someone has varying degrees of femoral torsion, tibial torsion or talar torsion. Each case is different, and each will be unique in their presentation and in the uniqueness of the treatment recipe. I just thought I would throw that in to make your head spin a little in case it wasn’t already.

For example, a case where the rearfoot is a semi rigid varus, with tibial varum, and frontal plane lateral pelvic drift with components of cross over gait (ie. the video case above) will require a different treatment plan and strategy than the same rearfoot varus in a presentation of femoral torsion challenges and genu valgum. Same body parts, different orientations, different mechanics, different treatment recipe.  

So, you can fiddle with a dozen pair of shoes to find one that helps minimize your pains, you can go for massages and hope for the best, you can go and get activated over and over, you can try yet another new orthotic, you can go to a running clinic and try some form changes, throw in some yoga or pilates, compression wear, voodoo bands and gosh who knows what else. Sometimes they are the answer or stumble across it … or you can find someone who understands the pieces of the puzzle and how to piece a reasonable recipe together to bake the cake just right. We do not always get there, but we try.  

Want more ? Try our National Shoe Fit certification program for a starter or try our online teleseminars at www.onlinece.com (we did a one hour course on the RearFoot just the other night, and it was recorded over at onlineCE.com).

Dr. Shawn Allen,  of the gait guys

Reference:

Man Ther.  2014 Oct;19(5):379-85. doi: 10.1016/j.math.2013.10.003. Epub 2013 Oct 29.Clinical measures of hip and foot-ankle mechanics as predictors of rearfoot motion and posture.  Souza TR et al.

Health professionals are frequently interested in predicting rearfoot pronation during weight-bearing activities. Previous inconsistent results regarding the ability of clinical measures to predict rearfoot kinematics may have been influenced by the neglect of possible combined effects of alignment and mobility at the foot-ankle complex and by the disregard of possible influences of hip mobility on foot kinematics. The present study tested whether using a measure that combines frontal-plane bone alignment and mobility at the foot-ankle complex and a measure of hip internal rotation mobility predicts rearfoot kinematics, in walking and upright stance. Twenty-three healthy subjects underwent assessment of forefoot-shank angle (which combines varus bone alignments at the foot-ankle complex with inversion mobility at the midfoot joints), with a goniometer, and hip internal rotation mobility, with an inclinometer. Frontal-plane kinematics of the rearfoot was assessed with a three-dimensional system, during treadmill walking and upright stance. Multivariate linear regressions tested the predictive strength of these measures to inform about rearfoot kinematics. The measures significantly predicted (p ≤ 0.041) mean eversion-inversion position, during walking (r(2) = 0.40) and standing (r(2) = 0.31), and eversion peak in walking (r(2) = 0.27). Greater values of varus alignment at the foot-ankle complex combined with inversion mobility at the midfoot joints and greater hip internal rotation mobility are related to greater weight-bearing rearfoot eversion. Each measure (forefoot-shank angle and hip internal rotation mobility) alone and their combination partially predicted rearfoot kinematics. These measures may help detecting foot-ankle and hip mechanical variables possibly involved in an observed rearfoot motion or posture.

Spinal interneuronal networks linking the forelimbs and hindlimbs

Do the intimate relationships of the upper limbs and lower limbs suggest that quadrupedal skill sets, if not true quadrupedal gait, were a piece of our past locomotion strategies ?  Or is it just representative of the close linkages for gait efficiency? Or maybe both?

In this study below the researchers pondered whether lower limb motor function can be improved after a spinal cord lesion by re-engaging functional activity of the upper limbs. Although this study looked at spinal cord hemisections in adult rats we know there is likely human correlation. This study showed improved hindlimb function when the forelimbs were engaged simultaneously with the hindlimbs during treadmill step-training as opposed to training only the hindlimbs.
As we have proposed here on the gait guys blog many times previously, this study’s results provide strong evidence that actively engaging the forelimbs improves hindlimb function and that one likely mechanism underlying these effects is the reorganization and re-engagement of rostrocaudal spinal interneuronal networks.
“For the first time, we provide evidence that the spinal interneuronal networks linking the forelimbs and hindlimbs are amenable to a rehabilitation training paradigm. Identification of this phenomenon provides a strong rationale for proceeding toward preclinical studies for determining whether training paradigms involving upper arm training in concert with lower extremity training can enhance locomotor recovery after neurological damage.”

This likely has huge implications in rehab measures and gait retraining for those who are not spinal cord impaired as well.  We have discussed many times that making a single limb change merely because the observer/clinician does not like the functional appearance of a limb is a  mistake most of the time. That what we see is a compensation, not the problem.  Go back and review our many “arm swing” blog posts, you should recall that the arms can have a huge impact on the leg function and that many times the arms take their cues from the lower limbs during gait.  This is a topic we have hammered many times in many blog posts and in many courses we have taught.  It is nice to see the literature continue to support the close relationships of the 4 limbs on a neurologic level.


Brain. 2013 Nov;136(Pt 11):3362-77. doi: 10.1093/brain/awt265. Epub 2013 Oct 7.

Use of quadrupedal step training to re-engage spinal interneuronal networks and improve locomotor function after spinal cord injury.

Shah PK1, Garcia-Alias G, Choe J, Gad P, Gerasimenko Y, Tillakaratne N, Zhong H, Roy RR, Edgerton VR.