Podcast 106: Understanding Tendonopathies & Asymmetrical Bone density in athletes.

* Plus the global effects of Hallux Limitus, & Chronic exposure to routine high-impact, gravitational loads afforded to the support limb preferentially improved bone mass and structure

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Other Gait Guys stuff

2 Podcast links: 



B. iTunes link:

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

D. other web based Gait Guys lectures:
Monthly lectures at : www.onlinece.com type in Dr. Waerlop or Dr. Allen, ”Biomechanics”

-Our Book: Pedographs and Gait Analysis and Clinical Case Studies
Electronic copies available here:


-Barnes and Noble / Nook Reader:


-Hardcopy available from our publisher:


Show Notes:

New device to get people with paralysis back on their feet
Scientists have tested the world’s first minimally-invasive brain-machine interface, designed to control an exoskeleton with the power of thought

Splicing out torsions, and aberrant foo types ? Club foot ? etc

Scientists Capture Crispr’s Gene-Cutting in Action

The UK Just Green-Lit Crispr Gene Editing in Human Embryos

Asymmetries in limbs

Tension or compression ?
link to full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3676165/

Concept: the forces have to go somewhere, it is a “passing the buck” system.  
We did this blog post here to explain:

The new muscle discovery !

tendinopathy vasculature: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650849/

tendinopathy treatment paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2505250/

Knee hyperextension and delayed heel rise in an interesting sport, Racewalking.

If you have been in practice long enough, you should know by now that in order to truly help an athlete you have to know their sport, the subtleties and the specifics.  You have heard us talk about premature heel rise off an on for years. Today, you must consider the opposite, delayed heel rise and the bizarre loading responses that come into the kinetic chains from such a behavior.

Racewalking is a long-distance event requiring one foot to be in contact with the ground at all times. Stride length is thus reduced and so to achieve competitive speeds racewalkers must attain cadence rates comparable to those achieved by Olympic 800-meter runners for hours at a time. Most people cannot truly appreciate how fast these folks are going.

There are really only two rules that govern racewalking:

1-The first rules states that the athlete’s trailing foot’s toe cannot leave the ground until the heel of the leading foot has created contact. 

2-The second rule specifies that the supporting leg must straighten, essentially meaning knee extension (and for some, terminal extension, ie. negative 5-10 degrees !) from the point of contact with the ground and remain straightened until the body passes directly over it. Again, essentially meaning full range knee extension for the entire stance phase of gait (early, mid and late midstance phases). 

Delated heel rise ?

Clearly some folks are going to take knee extension a little more literally. Look at the fella in the red and yellow. Can you say knee HYPER extension ? This is right knee anteriormeniscofemoral impingement looming on the horizon, this is an anterior compression overload phenomenon via the quadriceps. This is often met in this sport with the delayed heel rise that the sport seems to often drive. Prolonging the foot ground contact phase, attempting to abide by Rule#2, “the support  leg must straighten”, can lead to knee hyperextension if one is not careful. This will put a longer stretch load into the achilles and posterior compartment mechanism and this prolonged stretch-contract load can eventually lead to local pathology let alone in combination with the anterior knee compression we just eluded to. These folks will also be at risk for more anterior pelvic tilt, distraction of the anterior hip capsule-labral interval, unique hip extension and gluteal integration, and even possibly altered hip extension motor patterning driving abnormal loads into the hamstrings and low back.  Just imagine the changes in the hip flexor strategies in this scenario. 

To help your athletes, know their sport, know your normal biomechanics and know the pathologies when the rules of clean biomechanics are broken.

Today, on Rewind Friday, we will repost a more in-depth, with video, piece we did a few years ago on Race Walking. You may learn more about normal and abnormal gait than you think, today we translate some of the rules of the sport of race walking into deeper thoughts on gait mechanics.

Here is the link to our more in-depth video assessment and dialogue on the fascinating sport of race walking. If you have never truly looked at this sport before, you should enjoy this Rewind Post. (link).

– Dr. Shawn Allen

Not sure we agree this is the best direction. Imaging how much shoulder stability will be necessary. As least with the Axillary/rib cage crutch placement people can splint their arms and torso into a more stable tripod. The load is shared between the arm-shoulder and the torso. The thorax is taken out of the equation with this new design and that means 100% of the stability must come from the scap-thoracic and glenohumeral intervals. And, most people will not have the endurance stability capacity in those joints either. Sure, it has some great design principles, but we do not things all the variables have been taken into account. We see more shoulder problems coming out of this kind of crutch design. We feel pretty strongly about this. What do you guys think ?

Got Graft? Got ACL? Rehabbing one? This will give you some excellent insight.

An excellent read for folks wanting to know more about ACL grafts and outcomes.

Bottom line:
allografts (your own tissue) seem to fare better than autografts (cadaver tissue)

BPTB (bone patellar tendon bone) seem to have more longevity.

Read on here

Treat the paraspinals in addition to the peripheral muscle

As people who treat a wide variety of gait related disorders we often emphasize needling the paraspinal muscles associated with the segemental innervation of the peripheral muscle you are treating. For example, you may facilitate or needle the L2-L4 paraspinals (ie: femoral nerve distribution) along with the quads, or perhaps the C5-C6 PPD’s along with the shoulder muscles for the deltiods or rotator cuff for arm swiing. We do this to get more temporal and spacial summation at a spinal cord level, to hopefully get better clinical results.

White and Panjabi described clinical instability as the loss of the ability of the spine, under physiologic loads, to maintain relationships between vertebrae in such a way that there is neither damage nor subsequent irritation to the spinal cord or nerve roots, and, in addition there is no development of incapacitating deformity or pain due to structural changes.

Increased movement between vertebrae (antero or retrolisthesis) of > 3.5 mm (or 25% of the saggital body diameter) during flexion and/or extension suggests clinical instability. This often leads to intersegmental dysfunction and subsequent neurological sequelae which could be explained through the following mechanisms:

Recall that the spinal nerve, formed from the union of the ventral (motor) and dorsal (sensory) rami, when exiting the IVF splits into an anterior and posterior division, supplying the structures anterior and posterior to the IVF respectively. The posterior division has 3 branches: a lateral branch that supplies the axial muscles such as the iliocostalis and quadratus; an intermediate branch, which innervates the medial muscles, such as the longissimus, spinalis and semispinalis; and a medial branch, which innervates the segmental muscles, (multifidus and rotatores) as well as the joint capsule. Inappropriate intersegmental motion has 2 probable neurological sequelae: I) alteration of afferentation from that level having segmental (reflexogenic muscle spasm or vasoconstrictive/vasodilatory changes from excitation of primary afferents and gamma motoneurons) and suprasegmental (less cerebellar afferentation, less cortical stimulation) effects and II) compression or traction of the medial branch of the PPD, causing,  over time, demyelination and resultant denervation, of the intrinsic muscles, resulting in impaired motor control both segmentally and suprasegmentally. The segmental effects are directly measurable with needle EMG. This is a form of paraspinal mapping, which has also been explored by Haig et al. So, in short, instability can lead to denervation and denervation can lead to instability.

We often see clinically that treating a trigger point (needling, dry needling, acupuncture, manual pressure) can alter the function of the associated muscle . Improvements in muscle strength and changes in proprioception are not uncommon. Needling also seems to increase fibroblastic activty through the local inflammation it causes. Wouldn’t better muscle function and some scar tissue be a beneficial thing to someone with instability?

The next time you have a patient with instability, make sure to include the paraspinals in your quest for better outcomes.