A little neuro, anyone?

Welcome to Monday, and yes, it is a NEURO day. In fact, if you got up this morning, you too are having a NEURO day. Dr Allen thinks it’s all about the ORTHOPEDICS, but without NEURO, there would not be any orthopedics : )

A dialogue from one of our avid readers, Dr. Ryan.

Dr. Ryan: Hey Ivo,

I just read this article on Mercola’s site which is an interview with Dr. Craig Buhler who does muscle activation techniques.  Can you check this for accuracy?  This must be a mistake b/c I always thought spindle activation will facilitate the muscle to contract.  Also, I always wondered why the O/I attachment points are tender in muscles that are inhibited.  Does his description sound right to you.  If not, do you have a better explanation?

“Your muscle system and nervous system relate to each other from within tiny muscle fibers called spindle cells, which monitor stretch. If your muscle is overloaded too rapidly, the spindle cells will temporarily inhibit the muscle. The next time you contract the muscle, it will fire again. Similarly, cells within your tendons called Golgi tendon organs also measure and monitor stretch. If your tendon is stretched too rapidly or exceeds its integrity, the Golgi tendon organs will temporarily inhibit the muscle. But the next time the muscle fires, it will again fire appropriately.

“But there’s a fail-safe system,” Dr. Buhler explains. “It’s where the tendon attaches into the periosteum of the bone and the little fibers there are called Sharpey’s fibers. Those fibers are loaded with little receptors that monitor tension. And if the integrity of those fibers are exceeded, they inhibit the muscle, just like a circuit breaker would inhibit an electrical circuit.

Once that happens, the muscle will still fire under passive range of motion. But if you load the muscle, it gives way. If you continue to load the muscle, your body creates pain at the attachment points to protect you. What the central nervous system does at that point is compute an adaptive strategy by throwing stress into the muscle next to it. Other tissues begin to take on more of the load for the muscle that’s been injured.”

Here is a link to the entire article if you want to check it out:

http://fitness.mercola.com/sites/fitness/archive/2013/01/04/advanced-muscle-integration-technique.aspx?e_cid=20130104_DNL_art_1

Dr Ivo: Thanks Dr. Ryan.

Spindles monitor length and GTO’s monitor tension. My understanding is spindles, when activated, stimulate the alpha motor neuron(at the cord) and cause contraction of that muscle or motor unit. GTO’s, when activated, cause inhibition of the muscle they are associated with. I am not aware of them being inhibitory, only GTO’s. They are believed to be GABAnergic synapses. The impulse (at least in cats) can be smaller or inhibited if the muscle is held in contraction for an extended period of time (see attached)

Perhaps he is talking about spindle dysfunction, where the intrafusal portion of the spindle (which is innervated by a gamma motor neuron) is either excited or inhibited. The gamma’s are more of a slave to the interneuronal pool (in the cord), which would be the sum total of all excitatory and inhibitory input to that area (ie the central integrated state). This not only reflects local receptor input but also cortical information descending (from areas 4s and 6 in the precentral gyrus) AND descending information from the caudal reticular formation.

Based on what you sent, I do not agree with the 1st 2 sentences. I was not aware about increased receptor density of Sharpeys fibers. I did a quick search and found this: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2100202/  , which eludes to it and here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3098959/. I will have to dive in more when I have time.

Not sure why O/I attachments are tender in inhibited muscles. I find them tender in most folks. Maybe because inhibited muscles ave altered receptor function and that preloads the nociceptive afferent pathway or at least that neuronal pool? Are they closer to threshold for some reason? Not sure. LMK what you find.

Thanks for getting me jazzed about sharpeys fibers!

for those of you who need to know YES, there will be a forthcoming Sharpeys fibers article

Dr. Ryan: That’s what I thought.  Thanks for looking into it and I will check out those links.  You have jazzed me plenty of times over the years.  Glad I could jazz you up for a change.  Have a great weekend.


Yes, Dr Ivo is definitely an uber neuro geek, especially when he spends time on the weekend talking about spindles!



all material copyright 2013 The Homunculus Group/ The Gait Guys. All rights reserved. Please as before you lift our stuff.

A little neuro, anyone?

Welcome to Monday, and yes, it is a NEURO day. In fact, if you got up this morning, you too are having a NEURO day. Dr Allen thinks it’s all about the ORTHOPEDICS, but without NEURO, there would not be any orthopedics : )

A dialogue from one of our avid readers, Dr. Ryan.

Dr. Ryan: Hey Ivo,

I just read this article on Mercola’s site which is an interview with Dr. Craig Buhler who does muscle activation techniques.  Can you check this for accuracy?  This must be a mistake b/c I always thought spindle activation will facilitate the muscle to contract.  Also, I always wondered why the O/I attachment points are tender in muscles that are inhibited.  Does his description sound right to you.  If not, do you have a better explanation?

“Your muscle system and nervous system relate to each other from within tiny muscle fibers called spindle cells, which monitor stretch. If your muscle is overloaded too rapidly, the spindle cells will temporarily inhibit the muscle. The next time you contract the muscle, it will fire again. Similarly, cells within your tendons called Golgi tendon organs also measure and monitor stretch. If your tendon is stretched too rapidly or exceeds its integrity, the Golgi tendon organs will temporarily inhibit the muscle. But the next time the muscle fires, it will again fire appropriately.

“But there’s a fail-safe system,” Dr. Buhler explains. “It’s where the tendon attaches into the periosteum of the bone and the little fibers there are called Sharpey’s fibers. Those fibers are loaded with little receptors that monitor tension. And if the integrity of those fibers are exceeded, they inhibit the muscle, just like a circuit breaker would inhibit an electrical circuit.

Once that happens, the muscle will still fire under passive range of motion. But if you load the muscle, it gives way. If you continue to load the muscle, your body creates pain at the attachment points to protect you. What the central nervous system does at that point is compute an adaptive strategy by throwing stress into the muscle next to it. Other tissues begin to take on more of the load for the muscle that’s been injured.”

Here is a link to the entire article if you want to check it out:

http://fitness.mercola.com/sites/fitness/archive/2013/01/04/advanced-muscle-integration-technique.aspx?e_cid=20130104_DNL_art_1

Dr Ivo: Thanks Dr. Ryan.

Spindles monitor length and GTO’s monitor tension. My understanding is spindles, when activated, stimulate the alpha motor neuron(at the cord) and cause contraction of that muscle or motor unit. GTO’s, when activated, cause inhibition of the muscle they are associated with. I am not aware of them being inhibitory, only GTO’s. They are believed to be GABAnergic synapses. The impulse (at least in cats) can be smaller or inhibited if the muscle is held in contraction for an extended period of time (see attached)

Perhaps he is talking about spindle dysfunction, where the intrafusal portion of the spindle (which is innervated by a gamma motor neuron) is either excited or inhibited. The gamma’s are more of a slave to the interneuronal pool (in the cord), which would be the sum total of all excitatory and inhibitory input to that area (ie the central integrated state). This not only reflects local receptor input but also cortical information descending (from areas 4s and 6 in the precentral gyrus) AND descending information from the caudal reticular formation.

Based on what you sent, I do not agree with the 1st 2 sentences. I was not aware about increased receptor density of Sharpeys fibers. I did a quick search and found this: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2100202/  , which eludes to it and here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3098959/. I will have to dive in more when I have time.

Not sure why O/I attachments are tender in inhibited muscles. I find them tender in most folks. Maybe because inhibited muscles ave altered receptor function and that preloads the nociceptive afferent pathway or at least that neuronal pool? Are they closer to threshold for some reason? Not sure. LMK what you find.

Thanks for getting me jazzed about sharpeys fibers!

for those of you who need to know YES, there will be a forthcoming Sharpeys fibers article

Dr. Ryan: That’s what I thought.  Thanks for looking into it and I will check out those links.  You have jazzed me plenty of times over the years.  Glad I could jazz you up for a change.  Have a great weekend.


Yes, Dr Ivo is definitely an uber neuro geek, especially when he spends time on the weekend talking about spindles!



all material copyright 2013 The Homunculus Group/ The Gait Guys. All rights reserved. Please as before you lift our stuff.

Neuromechanics?  This early in the morning?

It has been a while since we have done a neuromechanics post. While doing some research for one of our PODcasts, We ran across this paper: http://www.ajronline.org/content/184/3/953.full

It’s title?

Midbrain Ataxia: An Introduction to the Mesencephalic Locomotor Region and the Pedunculopontine Nucleus

Yikes! What a mouthful!

What’s the bottom line?

The paper review a condition called “gait ataxia”. In plain English this means “aberrant or unsteady” gait. Things which usually cause gait ataxia originate in an area of the brain called the cerebellum, which coordinates all muscle activity. If you drink to much alcohol, it affects your cerebellum and you have a “wobbly” gait : ).

This paper looks at another area of the brain called the midbrain. It is the top part of the brainstem and contains an important gait integration and initiation center called the “midbrain locomotor nucleus”. The paper looks at 3 different cases and has some cool MRI images to see, along with alot of fancy neurological words and pathways.

Whenever we see gait ataxia, we think of impaired proprioception (look here for a bunch of posts on that, or at this post specifically).

There are many factors to consider when evaluating ataxic (or wobbly) gait, and this just gives us all one more place to look.

The Gait Guys. Making you smarter every day!

Neuromechanics Weekly: How does appropriate movement diminish pain?

We talk about proper (or should we say appropriate) movement (including gait) inhibiting or diminishing pain. So, how does that happen?

Above on the left is a great diagram that we will work through.

You are looking at a cross section of a spinal cord (We can hear the groans already!) We remember that the dorsal horn (posterior part) is sensory and the ventral horn (front) is motor. In between them (the lateral horn) is autonomic (this runs automatized body functions such as your heart, lung, guts, etc).

Small nerve fibers subserve pain. These are the A delta and C nerve fibers. “Small” refers to fiber diameter of the nerve. These nerves are where pain stimuli enters the spinal cord; they enter the sensory dorsal horn and synapse/connect there with the next neuron in line that takes the sensory message up the spinal cord to the brain to tell you about the pain including its intensity, location etc. Pain can result from tissue damage or injury (which can be due to, or the result of, poor biomechanics).

Large diameter nerve fibers subserve sensations like touch, pressure, vibration, muscle spindles (muscle length) and golgi tendon organs (muscle tension/load). These fibers also enter the sensory dorsal horn, but they do not synapse immediately, unlike pain fibers. They ultimately travel up to the top of the brainstem or cerebellum to coordinate information with other data your brain is processing. They send a branch (or collateral) to an inhibitory neuron, which excites the inhibitory neuron. Thus, if you excite an inhibitory neuron, it does it’s job and inhibits the propagation of an impulse. In this case, it inhibits the pain impulse from traveling to the cortex. So pain is inhibited. Appropriate biomechanics excite the largest population of receptors and provide the most effective response. 

Now look at the diagram on the right. It is a simplified schematic of the one on the left, with detail of the connections. Note that the LARGE FIBERS (from joint mechanoreceptors, spindles, muscles, etc) EXCITE the inhibitory interneuron (which would inhibit it). Also note that the SMALL FIBERS INHIBIT the inhibitory internuron (which would excite it!)

There you have it. Clear as mud? Go through some of our old posts on receptors and FEEL THE PAIN (parts 1, 2, 3+4) and come back to this and read it again. You know you want to be a geek, so go ahead!

The Gait Guys: Geeks on many levels. helping you to presynaptically inhibit pain on a daily basis, through better movement.