Abdominal Activity and Gait

We came across this cool study today, after a well educated patient asked about abdominal activity during gait.

Here is the bottom line:
low level activity in the rectus abdominis and external oblique throughout the gait cycle, more concentrated activity of the internal oblique at initial contact/loading response (heel strike).

This makes sense, since the external oblique occupies more real estate and has a larger cross sectional area; it most likely has a role in stabilization both in rotational like emoticon planes as well as the saggital plane (Z). Perhaps the action of the internal oblique at initial contact is to assist in external rotation of the pelvis on the stance phase leg, as the the opposite leg goes into swing?

“Cluster analysis identified two patterns of activity for the internal oblique, external oblique and rectus abdominis muscles. In the lumbar erector spinae, three patterns of activity were observed. In most instances, the patterns observed for each muscle differed in the magnitude of the activation levels. In rectus abdominis and external oblique muscles, the majority of subjects had low levels of activity (<5.0% of a maximum voluntary contraction) that were relatively constant throughout the stride cycle. In the internal oblique and the erector spinae muscles, more distinct bursts of activity were observed, most often close to foot-strike. The different algorithms used for the cluster analysis yielded similar results and a discriminant function analysis provided further evidence to support the patterns observed”

Clin Biomech (Bristol, Avon). 2002 Mar;17(3):177-84.
Abdominal and erector spinae muscle activity during gait: the use of cluster analysis to identify patterns of activity.
White SG1, McNair PJ.

Forefoot Varus Anyone?

Forefoot varus appears to move the center of gravity medially while walking. Nothing earthshaking here, but nice to see the support of the literature.

“The most medial CoP of the row and CoP% detected increased medial CoP deviation in FV ≥ 8°, and may be applied to other clinical conditions where rearfoot angle and CoP of the array after initial heel contact cannot detect significant differences.”

We will be talking about foot types this week on onlinece.com; Wednesday 8 EST, 7 CST, 6MST, 5 PST Biomechanics 314. Hope to see you there!

J Formos Med Assoc. 2015 May 5. pii: S0929-6646(15)00132-1. doi: 10.1016/j.jfma.2015.03.004. [Epub ahead of print]
Analysis of medial deviation of center of pressure after initial heel contact in forefoot varus.

picture from: http://forums.teamestrogen.com/showthread.php?t=46901

Clinical tidbit:

Heel pain in kids and adolescents? Have you considered Sever’s disease?

Apophysitis of the calcaneal apophysis is the most common cause of heel pain in adloscents and accounts for 8% of all pediatric overuse injuries! An apophysitis occurs (an injury involving a “pulling away” of bone from the tendons attachment site) because the strength of the tendon exceeds the strength of attachment of the tendon to the bone. It is most common in activites llike running, jumping and plantar flexion.

Gillespie H. Osteochondroses and apophyseal injuries of the foot in the young athlete. Curr Sports Med Rep 2010;9(5):265-268.

Wilson JC, Rodenburg RE. Apophysitis of the lower extremities. Contemp Pediatr 2011;28(6):38-46.

Ahh yes, the lumbricals. 

One of our favorite muscles. And here it is in a recent paper! This one is for all you fellow foot geeks : )

Perhaps the FDL (which fires slightly earlier than the FHL) and FHL (which fires slightly later and longer) at loading response, slowing pronation and setting the stage for lumbrical function from midstance to terminal stance/preswing (flexion at the metatarsal phalangeal joint (it would have to be eccentric, if you think about this from a closed chain perspective) and extension (actually compression) of the proximal interphalangeal joints.

“The first lumbrical arose as two muscle bellies from both the tendon of the FDL and the tendinous slip of the FHL in 83.3 %, and as one muscle belly from the tendon of the FDL or the tendinous slip of the FHL in 16.7 %. These two muscle bellies subsequently merged to form the muscle belly of the first lumbrical. The second lumbrical arose from the tendinous slips of the FHL for the second and third toes as well as the tendon of the FDL in all specimens. The third lumbrical arose from the tendinous slips of the FHL for the third and fourth toes in 69.7 %, and the fourth lumbrical arose from the tendinous slip of the FHL for the fourth toe in 18.2 %. Some deep muscle fibers of the fourth lumbrical arose from the tendinous slip of the FHL for the second toe in 4.5 %, for the third toe in 28.8 %, and for the fourth toe in 15.2 %.”

Hur MS1, Kim JH, Gil YC, Kim HJ, Lee KS. New insights into the origin of the lumbrical muscles of the foot: tendinous slip of the flexor hallucis longus muscle. Surg Radiol Anat. 2015 May 12. [Epub ahead of print]

Prior hamstring injuries

Previous hamstring injury is associated with altered biceps femoris associated muscle activity and potentially injurious kinematics.

“Previously injured athletes demonstrated significantly reduced biceps femoris muscle activation ratios with respect to ipsilateral gluteus maximus, ipsilateral erector spinae, ipsilateral external oblique, and contralateral rectus femoris in the late swing phase. We also detected sagittal asymmetry in hip flexion, pelvic tilt, and medial rotation of the knee effectively putting the hamstrings in a lengthened position just before heel strike.”
http://onlinelibrary.wiley.com/d…/10.1111/sms.12464/abstract

Foot “core” anyone?

And a good time was had by all. Day 1 of the event in Vancouver. Lots of info and a bonus exercise session. Thanks to all who attended and looking forward to another great day tomorrow!

We spent a great deal of time talking about muscular firing sequences and the reasoning as to why things fire when.

Take a look at the picture and focus on the tib posterior, flexor digitorum longus, and flexor hallucis longus. They fire from loading response and fire through terminal stance. Up to midstance, they act eccentrically to slow pronation and after midstance, they fire concentrically to assist in supination. Note the sequence starts with the tib posterior (more proximal attachments in the foot) and ends with the flexor hallucis longus, more distal attachements (because in “ideal” gait, the hallux is the last to leave the party (or the ground, in this case)). Stability is a priority, so the central or “core” of the foot needs to fire before adding on peripheral (appendicular) muscles. Remember the foot intrinsics fire from midstance to pre swing, further stabilizing the foot “core”

The Gait Guys

Attempting to regain a level playing ground for your foot.

“Remember, we were born with both our rearfoot and forefoot designed to engage on the same plane (the flat ground). We were not born with the heel raised higher than the forefoot. And, the foot’s many anatomically congruent joint surfaces, their associated ligaments, the lines of tendon pull and all the large and small joint movements and orchestrations with each other are all predicated on this principle of a rearfoot and forefoot on the same plane. This is how our feet were designed from the start.  This is why I like shoes closer to zero drop, when possible, because I know that we are getting closer to enabling the anatomy as it was designed. This is not always possible, feasible, logical or reasonable depending on the problematic clinical presentation and there is plenty of research to challenge this thinking, yet plenty to support is as well. The question is, can you get back to this point after years of footwear compensating ? Or have your feet just changed too much, new acquired bony and joint changes that have too many miles on the new changes ? Perhaps you have spent your first 20-50 years in shoes with heeled shoes of varying heel-ball offset. Maybe you can get back to flat ground, maybe you cannot, but if you can, how long will it take? Months ? Years ?  It all makes sense to me, but does it make sense for your feet and your body biomechanics after all these years ? Time will tell.” -Dr. Allen

Fundamental foot skills everyone should have, subconsciously. This video shows a skill you must own for good foot mechanics. It needs to be present in standing, walking, squatting, jumping and the like. It is the normal baseline infrastructure that you must have every step, every moment of every day. 

Is your foot arch weak ? Still stuffing orthotics and stability shoes up under that falling infrastructure ? Try rebuilding a simple skill first, one that uses the intrinsic anatomy to  help pull the arch up.  If your foot is still flexible, you can likely re-earn much of the lost skills, such as this one. This is a fundamental first piece of our foot, lower limb and gait restoration program. We start here to be sure this skill is present, then add endurance work on it and then eventually strength and gait progressions. This is where it starts for us gang. 

Shawn and Ivo, the gait guys

More muscle madness (or weakness, as the case may be)

In the last post (missed it? click here) , we discussed 3 causes of muscle weakness: local, segmental and cortical. In that post, we emphasized LOCAL causes of muscle weakness, determining that many of these causes related to direct injury, disease processes or neuromuscular endplate disorders.

This post will look at segmental causes, which as you have probably guessed, are at the spinal cord level. These are usually “electrical” problems, though in uncommon cases (syrinx, ependyoma, dermoid tumors) thay can be due to pathological processes. 

We need to understand that the spinal cord is composed of either tracts or nucleii, that’s pretty much it. The tracts are largely on the outside of the cord. Remember that they are the axons of nerves. Since they are myelinated (insulated), they are white in appearence. They have names like the spinocerebellar tracts, dorsal columns, reticulospinal tracts and corticospinal tracts, just to name a few. The nucleii are largely in the central part of the cord, organized in an “H” pattern that is divided up into layers called lamina. They are unmyelinated, so they are grey in appearance. Interspersed with these nucleii are perhaps one of the most important contributors to muscle weakness, the “interneurons” or “interneuronal pool”.

Remember, as impulses travel down from the cortex to control volitional (voluntary)movement, they end here in the internuncial pool and land on, you guessed it, interneurons. To this end, we need to remember that interneurons are 30X more numerous than any of the other cells in the central part of the cord. When a message is on its way down from the cortex, or heading up to it, most of the time, it interacts with an interneuron. In turn, interneurons can be excitatory or inhibitory. 

Something you should know about neurons, is that they are all or none. They either fire or they don’t. There is no in between. Same for interneurons. Depending on what they are connected to, the muscles (or autonomics, or other 2nd and 3rd order neurons) fire…or they don’t.

There are 2 types of motor neurons that go to muscle: alpha and gamma. Alpha motor neurons go to “extrafusal” muscle, or muscle we can control voluntarily. Gamma motor neurons go to “intrafusal” muscle, or muscle spindles, which monitor the length and rate of change of length of a muscle.

As you probably guessed, these motor neurons can be either activated directly (few) or through interneurons (many). These motor neurons connect with sensory neurons that monitor things like length, rate of change of length and tension in muscles. These modalities are subserved by receptors you have heard of: muscle spindles and golgi tendon organs. The alpha and gamma motor neurons also interact with axons of neurons that are descending from higher areas of the brain, like the cortex, cerebellum, vestibular nucleus, just to name a few.

It is the interplay of all these inputs and outputs, often referred to as the “central integrated state”, that ultimately determines whether a muscle fires or not, and thus if it is “weak” or “strong”. If excitation wins, then the nerve fires and the muscle contracts; if inhibition wins, then it does not. 

What are all the inputs and outputs? Only all the sensory and motor (this includes the autonomics ie sympathetic and parasympathetic) information arriving there from the periphery and central nervous system! Quite a lot!

Segmental causes, just another reason a muscle may test week

Ivo and Shawn: The Gait Guys