Can you see something strange in this gait ? You gotta look closely, there are several things that should bother you.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)

Not every gait problem is related to faulty shoes, bad feet or impaired arm swing.  

This is a case of CIDP that walked (terribly) into our clinic.  We did not initially know what this was but as you can see from this gait, if you look closely enough, something is just missing and wrong.

Arm swing is very problematic and there is no anti-phasic shoulder/pelvic girdle motions.  There are subtle demonstrations of both wide based gait steps and cross-overs. The gait is syncopated, sort of.  We had to shorten the clip for patient ID preservation, we wish we could have shown you more, it is really quite obvious that there is a systemic neurologic coordination problem in this patient.  With demyelinating polyneuropathies as the peripheral receptors become more and more impaired the brain eventually starts to lose more and more signals from the peripheral joints as to where the body parts are in space. IF the brain cannot find the parts, it cannot control them. If the brain just gets some of the signal the cerebellum cannot use its EFFERENT copy of the motor program, which is send out into the limbs, to orchestrate smooth coordinated tasks.  Go watch the video again, look at the global feel of the video, it is ratchety and syncopated.

CIDP is an acquired immune-mediated inflammatory disorder of the peripheral nervous system. The myelin sheath is slowly destroyed in this disease so nerve conduction is gradually lost. Some sources compare this disease to Guillian Barre disease. 

From wikipedia: 

Chronic inflammatory demyelinating polyneuropathy[3] is believed to be due to immune cells, cells which normally protect the body from foreign infection, but here begin incorrectly attacking the nerves in the body instead. As a result, the affected nerves fail to respond, or respond only weakly, to stimuli, causing numbing, tingling, pain, progressive muscle weakness, loss of deep tendon reflexes (areflexia), fatigue, and abnormal sensations. The likelihood of progression of the disease is high.

After seeing the client a few times, it was clear that there were several fixed neurologic parameters which could not be mediated and the client was sent an EMG/NCV and the specific diagnosis was made. The client was put on a monthly immunogloblulin IV drip and has remarkably stabilized.

Not all gaits are from a bad ankle, a slumbering cerebellum or cruddy arm swing.  Trust your clinical judgement, if it doesn’t feel right, refer up or laterally.  

Shawn and Ivo

A new twist on an old exercise

Do you know the the “Bird Dog” exercise? It looks like the picture above. The upper and contralateral lower extremities are extended, the the opposite ones are flexed. Seems to make make sense, unless you think about gait and neurology (yes, as you can see, those things seem to always be intertwined).

Think about gait. Your right leg and left arm flex until about midstance, when they start to extend; the left leg and right arm are doing the opposite. At no point are the arm and opposite leg opposing one another. Hmmm.

If you look at it neurologically, it is a crossed extensor reflex (see above); again, flexion of the lower extremity is paired with flexion of the opposite upper extremity. It is very similar to a protective reflex called the “flexor reflex” or “flexor reflex afferent”.

Wouldn’t it make more sense to do a cross crawl pattern? Or maybe like the babies shown above? Seems like if that’s the way the system was programmed, maybe we should try and emulate that. Don’t we want to send the appropriate messages to our nervous system for neurological re patterning? If you are doing the classic “opposite” pattern, what is your reasoning? Can you provide a sound neurological or physiological reason?

Think before you act. Know what you are doing.

The Gait Guys. Bridging the gap between neurology and gait, so you can do a better job.

Welcome to rewind (Late) Friday. Sorry about the late entry, folks.

Along the vein of bike fit, to go with our lecture on onlinece.com this week, here is gentleman with right sided low back pain ONLY when ascending hills on his mountain bike. Can you figure out why?

*Stop, watch the video and think about it before we give you the answer… .

____________________________

This gentleman presented with low back pain, only on his mountain bike, only on long ascents.

He measures out with an 83 cm inseam which should put him on a 44 to 45.5 cm frame (measured via our method). His frame has a dropped top tube and measures 55 cm.

He has a knee bend angle of 20 degrees at bottom dead center. Knee is centered well over pedal axis.

His stem falls far in front of his line of sight with respect to his hub. Stem is a 100 mm stem with a 6 degree rise.

There is a 2” drop from the seat to the top of the handlebars.

He has an anatomically short Left leg (tibial)

Look at the tissue folds at the waist and amount of reach with each leg during the downstroke.

The frame, though he is a big dude (6’+), is too big and his stem is too long. He is stretched out too far over the top tube, causing him to have an even more rounded back (and less access to his glutes; glutes should rule the downstroke and abs the upstroke). This gets worse when he pushes back (on his seat) and settles in for a long uphill. Now throw in a leg length discrepancy and asymmetrical biomechanics.

Our recommendations: smaller frame (not going to happen) lower seat 5-7mm shorter stem (60-75mm) with greater than 15 degree rise lift in Left shoe

We ARE the Gait Guys, and we do bikes too!

Go ahead and try this at home.remember last mondays post? (if not, click here). Here is one way of telling whether your (or someone else’s) vestibular system is working. It will also give you an idea of how some people compensate. Ready?
Stand up (barefoot or shoes does not matter).
place your hands resting on the top of your hips with your thumbs to the back (like your Mom used to, when you were in trouble). Your thumbs should be resting on your quadratus lumborum (QL) muscle. 
tilt your HEAD to the LEFT
you should feel the muscle (ie the QL) under your RIGHT thumb contract
come back upright
repeat, but this time lean your BODY to the LEFT
same thing right? Now check the other side.
Everything OK? Everything fire as it should?Now lets add another dimension.
slide your fingers down so they are just below the crest of the hip, resting above the greater trochanter (the bump on the side of your upper thigh). This should place your fingers on the middle fibers of the gluteus medius.
tilt your head (or body ) to the LEFT.
You should feel the LEFT gluteus medius and the RIGHT QL contract. These muscles should be paired neurologically. When walking, during stance phase on the LEFT: the LEFT gluteus medius helps to maintain the pelvis level, while the RIGHT QL, assists in hiking the RIGHT side.
If everything works OK, then your vestibulospinal spinal system is intact and your QL and gluteus medius seem to be firing and appropriately paired. If not? That is the subject for another post. The Gait Guys. Helping you to understand the concepts of WHY compensations occur.

Go ahead and try this at home.

remember last mondays post? (if not, click here). Here is one way of telling whether your (or someone else’s) vestibular system is working. It will also give you an idea of how some people compensate.

Ready?

  • Stand up (barefoot or shoes does not matter).
  • place your hands resting on the top of your hips with your thumbs to the back (like your Mom used to, when you were in trouble). Your thumbs should be resting on your quadratus lumborum (QL) muscle.
  • tilt your HEAD to the LEFT
  • you should feel the muscle (ie the QL) under your RIGHT thumb contract
  • come back upright


repeat, but this time lean your BODY to the LEFT

  • same thing right? Now check the other side.


Everything OK? Everything fire as it should?

Now lets add another dimension.

  • slide your fingers down so they are just below the crest of the hip, resting above the greater trochanter (the bump on the side of your upper thigh). This should place your fingers on the middle fibers of the gluteus medius.
  • tilt your head (or body ) to the LEFT.
  • You should feel the LEFT gluteus medius and the RIGHT QL contract. These muscles should be paired neurologically. When walking, during stance phase on the LEFT: the LEFT gluteus medius helps to maintain the pelvis level, while the RIGHT QL, assists in hiking the RIGHT side.


If everything works OK, then your vestibulospinal spinal system is intact and your QL and gluteus medius seem to be firing and appropriately paired. If not? That is the subject for another post.

The Gait Guys. Helping you to understand the concepts of WHY compensations occur.

Welcome to Rewind Friday, Folks. Today we review the importance of the great toe extensor. Enjoy!

Gait Topic: The Mighty EHB (The Short extensor of the big toe, do not dismiss it !)

Look at this beautiful muscle in a foot that has not yet been exposed to hard planar surfaces and shoes that limit or alter motion! (2 pics above, toggle back and forth)

The Extensor Hallicus Brevis, or EHB as we fondly call it (beautifully pictured above causing the  extension (dorsiflexion) of the child’s proximal big toe) is an important muscle for descending the distal aspect of the 1st ray complex (1st metatarsal and medial cunieform) as well as extending the 1st metatarsophalangeal joint. It is in part responsible for affixing the medial tripod of the foot to the ground.  Its motion is generally triplanar, with the position being 45 degrees from the saggital (midline) plane and 45 degrees from the frontal (coronal) plane, angled medially, which places it almost parallel with the transverse plane. With pronation, it is believed to favor adduction (reference). Did you ever watch our video from 2 years ago ? If not, here it is, you will see good EHB demo and function in this video. click here

It arises from the anterior calcaneus and inserts on the dorsal aspect of the proximal phalynx. It is that quarter dollar sized fleshy protruding, mass on the lateral aspect of the dorsal foot.  The EHB is the upper part of that mass. It is innervated by the lateral portion of one of the terminal branches of the deep peronel nerve (S1, S2), which happens to be the same as the extensor digitorum brevis (EDB), which is why some sources believe it is actually the medial part of that muscle. It appears to fire from loading response to nearly toe off, just like the EDB; another reason it may phylogenetically represent an extension of the same muscle.

*The EDB and EHB are quite frequently damaged during inversion sprains but few seem to ever look to assess it, largely out of ignorance. We had a young runner this past year who had clearly torn just the EHB and could not engage it at all. He was being treated for lateral ankle ligament injury when clearly the problem was the EHB, the lateral ligamentous system had healed fine and this residual was his chief problem.  Thankfully we got the case on film so we will present this one soon for you !  In chronic cases we have been known to take xrays on a non-standard tangential view (local radiographic clinics hate us, but learn alot from our creativity) to demonstrate small bony avulsion fragments proving its damage in unresolving chronic ankle sprains not to mention small myositis ossificans deposits within the muscle mass proper.

Because the tendon travels behind the axis of rotation of the 1st metatarsal phalangeal joint, in addition to providing extension of the proximal phalynx of the hallux (as seen in the child above), it can also provide a downward moment on the distal 1st metatarsal (when properly coupled to and temporally sequenced with the flexor hallicus brevis and longus), assisting in formation of the foot tripod we have all come to love (the head of the 1st met, the head of the 5th met and the calcaneus).

Wow, all that from a little muscle on the dorsum of the foot.

The Gait Guys. Definitive Foot Geeks. We are the kind of people your podiatrist warned you about…

Things may not always be how they appear.

What can you notice about all these kids that you may not have noticed before?

Look north for a moment. What do you notice about all the kids with a head tilt? We are talking about girl in pink on viewers left, gentleman in red 2nd from left, blue shirt all the way on viewers right. Notice how the posture of the 2 on the left are very similar and the one on the right is the mirror image?

What can be said about the rest of their body posture? Can you see how the body is trying to move so that the eyes can be parallel with the horizon? This is part of a vestibulo cerebellar reflex. The system is designed to try and keep the eyes parallel with the horizon. The semicircular canals (see above), located medial to your ears, sense linear and angular acceleration. These structures feed head position information to the cerebellum which then forwards it to the vestibular nucleii, which sends messages down the vestibulo spinal tract and up the medial longitudinal fasiculus to adjust the body position and eye position accordingly. 

Can you see how when we add another parameter to the postural position (in this case, running; yes, it may be staged, but the reflex persists despite that. Neurology does not lie), that there can be a compensation that you may not have expected?

What if one of these 3 (or all three) kids had neck pain. Can you see how it may not be coming from the neck. What do you think happens with cortical (re)mapping over many years of a compensation like this? Hmmm. Makes you think, eh?

Ivo and Shawn. The Gait Guys. Taking you a little further down the rabbit hole, each and every post.

The turned out foot. How far ahead (and how fast) can you think ? 
There are many causes of the turned out foot. The above slide is just one of many logical and possible chain of events.  
There are also reasons above the neck that cannot be ignored in creating the externally rotated foot (and in resolving it). Things are not always biomechanical in origin so remember this when you are continually doing activation and rehab interventions to get more glute or drive more internal limb spin and your results are met with a non-response.  
Most of us like a biomechanical line of thinking when it comes to apparent biomechanical aberrancies from the norm.  However, more often than you probably think (go back and listen to podcast 58 on Cortical Brain Mapping of injuries), several more purely neurologic reasons are plausible.  For example, changes in input/output in unilateral activity within the pontomedullary reticular formation (PMRF) of the brain can lead to inhibition of the posterior chain muscles below the T6 spinal level (And anterior muscles above T6. And what is awesome is that there are ways to test this kinda stuff on a physical exam !  However, this blog post is not the place to teach these neurologic examination procedures.  But, if this sounds like Janda’s Upper and Lower Crossed Syndromes you are thinking soundly. Just remember though, if you are fixing what you see, you may not be fixing the problem, fix the cause that drove what you are seeing.  If you know your functional neurology you will know where these things come from, they are a cortical phenomenon).  
Of the posterior compartment muscles below T6, the gluteus maximus is probably the largest of this group and when it is inhibited there is loss of control of its ability to stabilize single leg stance.  One strategy around a stability challenge would be to turn the foot/leg into the frontal plane (toe out) via external limb rotation.  Now we can use the remaining muscles in both the sagittal and frontal planes ! We are always more stable when we can engage two or more cardinal planes at the same time.
There are  many more reasons for the externally rotated limb/foot, for example vestibular dysfunction, cerebellar dysfunction, core dysfunction, impaired normal arm swing and the list goes on. We have talked about many of these reasons on many of our blog posts and podcasts.
Mental gymnastics when it comes to the brain are important, Keep your gait and human movement game sharp, work through scenarios in your head regularly because it is what is necessary when you are working up a client.  
Shawn and Ivo
the gait guys

The turned out foot. How far ahead (and how fast) can you think ? 

There are many causes of the turned out foot. The above slide is just one of many logical and possible chain of events.  

There are also reasons above the neck that cannot be ignored in creating the externally rotated foot (and in resolving it). Things are not always biomechanical in origin so remember this when you are continually doing activation and rehab interventions to get more glute or drive more internal limb spin and your results are met with a non-response.  

Most of us like a biomechanical line of thinking when it comes to apparent biomechanical aberrancies from the norm.  However, more often than you probably think (go back and listen to podcast 58 on Cortical Brain Mapping of injuries), several more purely neurologic reasons are plausible.  For example, changes in input/output in unilateral activity within the pontomedullary reticular formation (PMRF) of the brain can lead to inhibition of the posterior chain muscles below the T6 spinal level (And anterior muscles above T6. And what is awesome is that there are ways to test this kinda stuff on a physical exam !  However, this blog post is not the place to teach these neurologic examination procedures.  But, if this sounds like Janda’s Upper and Lower Crossed Syndromes you are thinking soundly. Just remember though, if you are fixing what you see, you may not be fixing the problem, fix the cause that drove what you are seeing.  If you know your functional neurology you will know where these things come from, they are a cortical phenomenon).  

Of the posterior compartment muscles below T6, the gluteus maximus is probably the largest of this group and when it is inhibited there is loss of control of its ability to stabilize single leg stance.  One strategy around a stability challenge would be to turn the foot/leg into the frontal plane (toe out) via external limb rotation.  Now we can use the remaining muscles in both the sagittal and frontal planes ! We are always more stable when we can engage two or more cardinal planes at the same time.

There are  many more reasons for the externally rotated limb/foot, for example vestibular dysfunction, cerebellar dysfunction, core dysfunction, impaired normal arm swing and the list goes on. We have talked about many of these reasons on many of our blog posts and podcasts.

Mental gymnastics when it comes to the brain are important, Keep your gait and human movement game sharp, work through scenarios in your head regularly because it is what is necessary when you are working up a client.  

Shawn and Ivo

the gait guys

Podcast 58: Brain Mapping Injuries, Muscle Activation & Sleep

The intricacies of how the brain maps a compensation pattern.

A. Link to our server:

Direct Download: 

http://traffic.libsyn.com/thegaitguys/pod_58f.mp3

Permalink: 

http://thegaitguys.libsyn.com/podcast-58-brain-mapping-injuries-muscle-activation-sleep

B. iTunes link:

https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138

C. Gait Guys online /download store (National Shoe Fit Certification and more !) :

http://store.payloadz.com/results/results.aspx?m=80204

D. other web based Gait Guys lectures:

www.onlinece.com   type in Dr. Waerlop or Dr. Allen,  ”Biomechanics”

_______________
Today’s Show notes:
Neuroscience pieces:
1. Gait Posture. 2013 Jul;38(3):549-51. doi: 10.1016/j.gaitpost.2013.02.008. Epub 2013 Mar 11.

Altered gait termination strategies following a concussion.

2. lack of sleep, brain damage……… honor  your recovery days and as importantly, honor the things that make you a better runner, that includes sleep !!!!!

4. New minimalist casual shoes:

Zed’s
Well, how convenient. A fantastic picture for teaching from the cover of one of our favorite magazines.
For this post, lets start with the gal on the left in the pink shirt. 1st of all, she is running in flip flops. Since these require so much long flexor activity to keep them on, not the best footwear choice, in our opinion. Check out that exaggerated left sided arm swing. This goes to propel herself forward. Why the extra effort? Check out her right (stance phase leg). What do you see? The knee points outward while the foot is planted. We are looking at either external tibial torsion or a femoral retrotorsion. Did you pick up the compensatory head tilt to the left? The vestibular system has become involved, and the trapezius and levator scapula seem to be it’s target (thus the shoulder hike and ipsilateral rotation), as well as the ipsilateral lateral benders and rotators of the cervical spine, namely the splenius cervicis and capitis (the multifidus/rotatores are contralateral rotators).
How about the subtle pelvic shift to the right? and the mild crossover gait (note the adduction of the left knee across midline).
It would be great to see a shot of her barefoot to see what changes, as increased long flexor activity has both local (impaired ankle rocker, excessive forefoot inversion, reciprocal inhibition of the anterior compartment muscles of the lower leg) as well as long distance (namely increased flexor drive to the brainstem and cerebellum) implications. We would want to see this (as well as examine her) before making any recommendations other than LOSE THE FLIP FLOPS GIRLFRIEND.
Wow, all that and we have only scratched the surface.

We remain the geeks of gait: Ivo and Shawn

Well, how convenient. A fantastic picture for teaching from the cover of one of our favorite magazines.

For this post, lets start with the gal on the left in the pink shirt. 1st of all, she is running in flip flops. Since these require so much long flexor activity to keep them on, not the best footwear choice, in our opinion. Check out that exaggerated left sided arm swing. This goes to propel herself forward. Why the extra effort? Check out her right (stance phase leg). What do you see? The knee points outward while the foot is planted. We are looking at either external tibial torsion or a femoral retrotorsion. Did you pick up the compensatory head tilt to the left? The vestibular system has become involved, and the trapezius and levator scapula seem to be it’s target (thus the shoulder hike and ipsilateral rotation), as well as the ipsilateral lateral benders and rotators of the cervical spine, namely the splenius cervicis and capitis (the multifidus/rotatores are contralateral rotators).

How about the subtle pelvic shift to the right? and the mild crossover gait (note the adduction of the left knee across midline).

It would be great to see a shot of her barefoot to see what changes, as increased long flexor activity has both local (impaired ankle rocker, excessive forefoot inversion, reciprocal inhibition of the anterior compartment muscles of the lower leg) as well as long distance (namely increased flexor drive to the brainstem and cerebellum) implications. We would want to see this (as well as examine her) before making any recommendations other than LOSE THE FLIP FLOPS GIRLFRIEND.

Wow, all that and we have only scratched the surface.

We remain the geeks of gait: Ivo and Shawn

Activation, Cortical Remapping and what you are doing wrong to your people.

We are getting ready to step back into the studio to record podcast 58. We have been touching upon this topic off and on in the last 2 podcasts and we are going back in for more on pod #58 because this stuff is just too important not to beat it to a further pulp.  

The gist of this article is that cortical remapping occurs with injuries that are not 100% resolved. Lots of coaches and trainers out there are trying their hands at muscle “activation” and other new trendy tricks and they are missing the boat and making people worse if they are not doing a good sound clinical history and examination. You can activate any muscles and get what appears to be a miracle response, we can teach a 8 year old how to do activation and get a miracle response, but is it the right response or have you created a temporary compensation for your client (right before you send them into training or competition) ?  Activation is a 2 way street, there is the input into the brain and a corresponding motor output. If you are just rubbing out some muscles and get a stronger muscle test afterwards, and that is as far as your thoughts go before you turn your athlete loose, then you are a liability in the system. Are you part of the problem or part of the solution ?

Here are 2 paragraphs from this brilliant article. This is worth your time. As a client adapts to their unresolved, partially resolved (yes, even 95% is unresolved) injury(s) a secondary cascade of neurological changes ensue that often force new cortical remapping.  A remapping that is not as fundamentally safe or as sound as the pre-injury mapping yet one that is necessary for protecting further or other injuries. Yet, because it is not the original pristine pattern, it is also one that can begin undercurrents to corrupt other patterns of stability, mobility and movement in cortical and subcortical mappings. Understanding cortical excitability is important, and it can work for you and your client or against you both. It can be used for good or evil.  

If after you read these 2 paragraphs taken from the Alan Needle article in LER (link) you think you might be part of the problem or realize that you are not the magician you think you are, then good, you are on the track to self enlightenment and actually helping people.  Go read Alan’s article and breathe deep, ready to absorb and start yourself into understanding that you are really fixing the brain and not always the muscle, and that means you are gonna have to learn about the brain and how it works and more so how it can deceive you and your client and your training, treatments or therapy.

Come join us on The Gait Guys podcast 58 later this week as we delve into this topic deeper and more broadly.

Shawn and Ivo

PS: nice article Dr. Needle. Thank you !

http://lowerextremityreview.com/article/the-brain-a-new-frontier-in-ankle-instability-research

"Recently Wikstrom and Brown proposed a hypothetical cascade of events that would affect an individual’s ability to “cope” following an ankle sprain and provide a rationale for the varying contributors to instability. For an individual starting from a point of normal function, a lateral ankle sprain will trigger a consistent pattern of changes to the joint from the inflammatory process. Swelling will increase pressure on the joint’s mechanoreceptors, and pain will contribute to inhibition of the reflexes to the joint (arthrogenic inhibition). Together, this means patients will have difficulty sensing the joint and subsequently stabilizing it while excessive mechanical laxity will increase this loss of stability.19

Inflammatory changes may be similar across all patients; however, as symptoms remain and the patient adapts after his or her injury, a secondary cascade of neurological changes may occur that may include cortical remapping. In some patients, these adaptations may be beneficial and serve to protect the joint from further injury. Other patients may maladapt, as sensorimotor reorganization changes the nervous system’s perception of the joint. Variable amounts of laxity, proprioception, and cortical excitability exist throughout populations of healthy, previously injured, and functionally unstable joints. Where these populations diverge may be related to how each is scaled relative to the others. For instance, a joint with greater amounts of laxity may have higher proprioception and excitability to aid in stabilizing the joint, but following injury, these factors may become decoupled, leading to errors in movement and coordination.19”  -Alan Needle, PhD

 

More on EVA foam, impact loading behaviors, and adding shoe inserts.

A few weeks ago we wrote about some thoughts on the maximalist shoe foam trend and how it is possible that more foam could mean alterations in impact loading behaviors that could lead to problems (note we used the word could, and not will).  If there are pre-existing proprioceptive deficits in a limb these issues most likely will rise to the surface. 

The EVA foam in shoes is primarily used to absorb forces via air flow through interconnected air cells in the EVA during shoe deformation under body-weight. When the shoe has seen a finite number of compressive cycles the air cells collapse and the EVA can compact on itself leaving the shoe with an negatively impacting area of compression to fall into.  Shock absorption may be impacted and possibly lead to injury.

The Robbins study we discussed a few weeks ago (link) suggested that the reduction of impact moderating behaviour is 

Reduction of impact-moderating behavior is a response to loss of stability induced by soft-soled cushioned shoes: Humans reduce impact-moderating behavior in direct relation to increased instability.This is presumably an attempt to achieve equilibrium by obtaining a stable, rigid support base through compression of sole materials. Humans reduce impact-moderating behavior, thereby amplifying impact, when they are convinced that they are well protected by the footwear they are wearing. 

These were important points but we wanted to bring to your awareness of the component of the shoe you may have not thought of to this point, the foam foot bed that comes with the shoe, or ones you might add to the shoe  yourself post-purchase. With what we have just taught you in our last blog post and this blog post, we will let you make the connection we are suggesting you be aware of when it come to more foam, changes in foam as the shoes and inserts degrade and impaired impact loading behaviors.

There are just 3 brief study summaries here, take the time to read them and read between the lines now that we have educated you a little better in how to think about them.

Shawn and Ivo

J Appl Biomech. 2007 May;23(2):119-27.

Effects of insoles and additional shock absorption foam on the cushioning properties of sport shoes.

The purpose of this study was to investigate the effects of insoles and additional shock absorption foam on the cushioning properties of various sport shoes with an impact testing method. 

The results of this study seemed to show that the insole or additional shock absorption foam could perform its shock absorption effect well for the shoes with limited midsole cushioning. 

Further, our findings showed that insoles absorbed more, even up to 24-32% of impact energy under low impact energy. 

It seemed to indicate that insoles play a more important role in cushioning properties of sport shoes under a low impact energy condition.

_______

Biomed Mater Eng. 2006;16(5):289-99.

Role of EVA viscoelastic properties in the protective performance of a sport shoe: computational studies.

 Using lumped system and finite element models, we studied heel pad stresses and strains during heel-strike in running, considering the viscoelastic constitutive behavior of both the heel pad and EVA midsole. In particular, we simulated wear cases of the EVA, manifested in the modeling by reduced foam thickness, increased elastic stiffness, and shorter stress relaxation with respect to new shoe conditions. Simulations showed that heel pad stresses and strains were sensitive to viscous damping of the EVAWear of the EVA consistently increased heel pad stresses, and reduced EVA thickness was the most influential factor, e.g., for a 50% reduction in thickness, peak heel pad stress increased by 19%. We conclude that modeling of the heel-shoe interaction should consider the viscoelastic properties of the tissue and shoe components, and the age of the studied shoe.

________________

J Biomech. 2004 Sep;37(9):1379-86.

Heel-shoe interactions and the durability of EVA foam running-shoe midsoles.

A finite element analysis (FEA) was made of the stress distribution in the heelpad and a running shoe midsole, using heelpad properties deduced from published force-deflection data, and measured foam properties. The heelpad has a lower initial shear modulus than the foam (100 vs. 1050 kPa), but a higher bulk modulus. The heelpad is more non-linear, with a higher Ogden strain energy function exponent than the foam (30 vs. 4). Measurements of plantar pressure distribution in running shoes confirmed the FEA. The peak plantar pressure increased on average by 100% after 500 km run. Scanning electron microscopy shows that structural damage (wrinkling of faces and some holes) occurred in the foam after 750 km run. Fatigue of the foamreduces heelstrike cushioning, and is a possible cause of running injuries.

 

Remember this kiddo?

We have been following the natural development of this little guy for some time now. For a review, please see here (1 year ago) and here (2 years ago) for our previous posts on him.

In the top 2 shots, the legs are neutral. The 3rd and 4th shots are full internal rotation of the left and right hips respectively. The last 2 shots are full external rotation of the hips.

Well, what do you think now?

We remember that this child has external tibial torsion and pes planus. As seen in the supine photo, when the knees face forward, the feet have an increased progression angle (they turn out). We are born with some degree / or little to none, tibial torsion and the in-toeing of infants is due to the angle of the talar neck (30 degrees) and femoral anteversion (the angle of the neck of the femur and the distal end is 35 degrees).  The lower limbs rotate outward at a rate of approximately 1.5 degrees per year to reach a final angle of 22 degrees….. that is of course if the normal de rotation that a child’s lower limbs go through occurs timely and completely.

He still has a pronounced valgus angle at the the knees (need a review on Q angles? click here). We remember that the Q angle is negative at birth (ie genu varum) progresses to a maximal angulation of 10-15 degrees at about 3.5 years, then settles down to 5-7 degrees by the time they have stopped growing. He is almost 4 and it ihas lessend since the last check to 15 degrees.

His internal rotation of the hips should be about 40 degrees, which it appears to be. External rotation should match; his is a little more limited than internal rotation, L > R. Remember that the femoral neck angle will be reducing at the rate of about 1.5 degrees per year from 35 degrees to about 12 in the adult (ie, they are becoming less anteverted).

At the same time, the tibia is externally rotating (normal tibial version) from 0 to about 22 degrees. He has fairly normal external tibial version on the right and still has some persistent internal tibial version on the left. Picture the hips rotating in and the lower leg rotating out. In this little fellow, his tibia is outpacing the hips. Nothing to worry about, but we do need to keep and eye on it.

What do we tell his folks?

  • He is developing normally and has improved significantly since his original presentation to the office
  • Having the child walk barefoot has been a good thing and has provided some intrinsic strength to the feet
  • He needs to continue to walk barefoot and when not, wear shoes with little torsional rigidity, to encourage additional intrinsic strength to the feet
  • He should limit “W” sitting, as this will tend to increase the genu valgus present
  • We gave him 1 leg balancing “games” and encouraged agility activities, like balance beam, hopping, skipping and jumping on each leg individually

We are the Gait Guys, promoting gait and foot literacy, each and every post.

Podcast 57: The Brain, Ankle Instability, Heel Striking

A. Link to our server:

Direct Download: 

http://traffic.libsyn.com/thegaitguys/pod_5777final.mp3

Permalink: 

http://thegaitguys.libsyn.com/podcast-57-the-brain-ankle-instability-heel-striking

B. iTunes link:

https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138

C. Gait Guys online /download store (National Shoe Fit Certification and more !) :

http://store.payloadz.com/results/results.aspx?m=80204

D. other web based Gait Guys lectures:

www.onlinece.com   type in Dr. Waerlop or Dr. Allen,  ”Biomechanics”

________________________________________

* Today’s show notes:

Neuroscience

Focus on BDNF: Brain Derived Neurotrophic Factor and Gait

http://www.ncbi.nlm.nih.gov/pubmed/10868966

Diabetes. 2000 Mar;49(3):436-44.
Brain-derived neurotrophic factor regulates glucose metabolism by modulating energy balance in diabetic mice.

http://ep.physoc.org/content/94/12/1153.full

Experimental Physiology –
Hot Topic Review
Role of exercise-induced brain-derived neurotrophic factor production in the regulation of energy homeostasis in mammals

The Brain: A new frontier in ankle instability Research
http://lowerextremityreview.com/article/the-brain-a-new-frontier-in-ankle-instability-research

Young Girls and Future injury risk.
http://lowerextremityreview.com/news/in-the-moment-sports-medicine/neuromuscular-training-in-young-girls-boosts-skills-may-reduce-future-risks

PRP review:
http://lowerextremityreview.com/news/in-the-moment-sports-medicine/platelet-rich-progress-data-support-prp-use-for-heel-pain

case: gait guys,

so i got orthotics which hurt like crazy (only on my bad foot). these were not the answer for me. i have an appointment with a hip specialist to see if my  … .
phil

DISCLAIMER

elliptical questions: 
Tried searching your blog but did not find anything on ellipticals.

What correct position is needed to use the machine?
I assume one that would take you out of the anterior pelvic tilt?
By doing this, would that enable  … . 
Q  :)

Alternative office furniture to avoid sitting at a desk all day
http://www.latimes.com/health/la-he-healthy-workplace-desks-20140222,0,5603953.story

Heel Landing Beats Midfoot In Half-Marathon Study
http://www.runnersworld.com/running-tips/heel-landing-beats-midfoot-in-half-marathon-study