Saturday, July 20, 2019

Treating cutaneous nerves and reducing muscle hypertonicity: What's the connection?

This question was posed to me in the DNM group on Facebook a few days ago. It's worth a blog post, I'm sure, because way too many practitioners out there in the big wide world still think they must have magic hands or something, and their instructors never explained to them that they don't.

Here was the question: 

I will reproduce my answer and alter it slightly so that it contains (I hope..) more clarity and expand it with links.

The whole physical basis of DNM is neurodynamics, as treatment described by Butler and Shacklock (although they only discussed long deep nerves), plus neurodynamics, as normal nerve movement as described by Lundborg in his nook, Nerve Injury and Repair, 1988

It's important to realize there are two definitions for "neurodynamics":
1. the "normal" "physiological" movement of nerves through neural tunnels, with ordinary active movement as so well-described by Lundborg in his book, Nerve Injury and Repair, from 1988, with all its gorgeous, rich illustrations
2. the "applied" "treatment" kind, defined by Michael Shacklock in his pivotal 1995 paper, "Neurodynamics" (Type the word into the box and click on the teeny box beneath to read the full paper, or download here instead.)  

... I like to think of nerves as information highways inside tubes throughout the body - 72 kilometers of them. The cutaneous nerves are fascicles branching away from the deeper named nerves, as are the motor branches, even though the motor branches are not usually given their own names the way cutaneous branches are. If you think of a highway in normal driving life, let's call it Highway 315, it would be like exit 42 goes to a muscle; the branch to the muscle contains motor neurons, but the name of that branch isn't separate from the name of the nerve itself (which is odd in my view, but oh well..). So we say, Highway 315 innervates the blahblah muscle, or even several muscles.
The nomenclature of peripheral nerves has always been biased in favour of the motor function of the nervous system. Even though ALL the main peripheral nerves are "mixed" (both sensory and motor), only cutaneous nerve branches are selected out for being "different" enough to get specific names. Motor branches of peripheral nerves do not.
From one perspective, this makes cutaneous nerves easier to learn from an anatomy text.
From another perspective, it can present a cognitive chasm - how does handling affect motor output? Pain output?
For manual therapists, it means that to understand how our handling affects nerves/nervous system we have to delve a lot deeper into the body of knowledge and are forced to be more rational

From this wonderful youtube video with Rafe Kelley and John Vervaeke, about minute 51

Back to the answer to the question:

But then we have exit 73. As soon as you take that exit, you find yourself on a "new" highway with a "new" name, maybe "Lake Road" or something. It's a different branch of the same big nerve, but it goes away from muscle instead of into it, doesn't contain any motor neurons, only autonomic motor neurons and sensory neurons, and it goes to skin. 

I want to rename this highway branch, "Vista View Road."
It doesn't go to a lake, it goes out to skin, and skin is open to the world.
To the environment.
These nerves pick up on everything out there.
Ambient temperature, breezes, contact with the planet through the soles of the feet.
Furthermore one can argue that special senses also have "skin" or at least, specialized membrane containing receptive neurons for picking up on light levels, different noises, different scents in the air depending on what season we are in, humidity levels, all sorts of inputs that are mainly subliminal and are handled efficiently by very old predictive processing systems in our central nervous system.
But I digress.
And I got carried away with the sensory function in cutaneous nerves. Lest we forget, they also contain numerous autonomic neurons, which are sympathetic, which are motor, and which regulate all the enormous vascular function of the skin organ, which contains 10 times more blood supply than needed for its own metabolic function, acting as a reservoir for emergencies and a thermodynamic regulatory organ for keeping body temperature within the narrow optimal homeostatic range necessary for life processes in mammals (of which we are a kind). I learned all this from reading Gray's Anatomy.
And I digressed again.
Back to the original answer: 

With me so far? 
Now, imagine that you can put your hand on "Lake Road", and physically move it, because it's embedded right into the underneath side of the skin! It's got its own fascicle inside the tubular Highway 315! When you move the skin, you move that fascicle (physically) all the way up Highway 315 (or at least a long way up it), and even, in fact (sensorially), all the way up to the brain. 

This is an important manual therapy concept to get: imagine pulling a string through a tube.
Imagine the tube (which is the peripheral nerve itself, containing lots of strings) goes all the way to the spinal cord.
Imagine the string you pull is easy enough to pull because it embeds right into the skin (organ), which you can "KNOW" (for a fact!) that you can get your hand directly on and move.
Plus, you are activating all kinds of computational low-threshold mechanoreceptors right at the skin organ surface. Of course the brain will know that someone is touching its organism, and how. 


This might be where Descartes got off track thinking there were specific "pain" neurons going to the brain. The thick heavily myelinated low-threshold A-beta mechanoreceptive neurons in skin certainly do - they go up the dorsal columns of the spinal cord to dorsal column nuclei in the medulla, synapse there, cross over, synapse again in the thalamus, and end up in the primary somatosensory cortex with high fidelity.
Nociceptive-capable, high-threshold neurons end in the dorsal horn of the spinal cord.
Well, unless they are A-delta nociceptive neurons, which are a bit thicker and faster with a bit more myelination, seem to have a lot more sensory-discriminative capacity, and are usually well and quickly inhibited.
See link.
And I digressed yet again.

(Furthermore, "Lake Road" has multiple turnoffs that go straight to the skin organ's surface, called rami, each inside its own little tube called a skin ligament!)
Yes. I took pictures of them.
With special permission.
Specifically, these are cutaneous rami of the lateral cutaneous nerve of the forearm (highlighted with a black felt marker).
I did this dissection in 2007 at UBC.
See Nash 2004 for a description of skin ligaments. 


Anatomically things are a lot more complex of course, fascicles anatomose and diverge right inside the nerve, and nerves themselves diverge and anastomose inside the plexuses from which they differentiate, etc.. PLUS all these fascicles have blood vessels going into them from accompanying arteries and out of them into accompanying veins and all this attached vasculature will ALSO be moved a little.

To see images of all this anastomosing business, plus neurodynamic elongation of nerve fascicles, go here

AND (we hope) moving said vasculature can mechanically affect, for the better (we hope!), said vascular function within the nerve (intraneural blood flow). Particularly if there is local pain, which MAY be a tunnel issue secondary to insufficient drainage/consequent intraneural engorgement/entrapment. 
But be all that as it may, Lundborg showed that fascicles can slide a bit to afford nerve elongation (sort of like a telescope can elongate by its inner parts sliding outward). 
And Butler and Shacklock (and whoever came along before they did) took these ideas and pain science at the time (late 80's, early 90's) and developed nerve sliding etc. as a treatment approach. Neither one of them worried much about cutaneous nerves, however, which is where I picked up the ideas and have included neurodynamics in treatment approaches to skin, i.e., moving of cutaneous nerves and their multiple rami, 1.) not just trying to have a sensory influence on the brain via skin receptors (although that is responsible for a lot of treatment effect), 2.) completely eliminating all irrelevant operative erroneous superfluous assumptions (still floating around like stinking bloated corpses in the river of ideas... 🙄👎 ) imagining we could possibly in a billion years affect mesodermally derived tissue (e.g., the myo, or the fascia..) directly
Then after some time had elapsed, I realized I still had not addressed the actual question:


Gad, I wrote all that stuff but didn't get around to answering the question did I? >>> "I have not found a concrete explanation as to how affecting the cutaneous nerves reduces hypertension in a muscle. So, what is the mechanism?"The only mechanism that has a ton of research to back it up is "non-specific effects", more specifically, top-down "descending modulation" by the brain, of the spinal cord. The brain's usual order of business is to inhibit gross spinal cord reflexive behavior. It's like the spinal cord thinks its job is to make everything BIG and the brain's job is to say, now now, not so big, and not right now. Remember the spinal cord can elicit withdrawal reflex in response to nociceptive input BEFORE the brain even registers a problem (i.e., be VERY protective. Maybe even over-protective.) (Plus the spinal cord came along earlier than the rest of the CNS so it tries to play the seniority card I suspect.)
Anyway, 50 years after Melzack and Wall's paper on gate control theory, a paper came out in 2015 that afforded it some direct evidence. (Foster et al 2015, see link) so there is now a shred of support for a bit of bottom-up inhibition of nociception as well. 

The Foster et al. paper is here


I added a bit later on in the thread that is my hunch (can't find any definitive reference for it yet) about why muscle hypertonicity occurs, even though it irritates the heck out of peripheral nerves that may be getting squeezed on in the process. 

From this thread

I hope this rounds out the discussion a bit more.


1. Shacklock, M. (1995). Neurodynamics. Physiotherapy, 81(1), 9–16. doi:10.1016/s0031-9406(05)67024-1
2. Neurodynamic Solutions 20th Anniversary Newsletter, "Nerve movement in 2015 - 20th Anniversary of neurodynamics in physical and manual therapy." Contains nerve movement video showing proof of concept and download link to full Neurodynamics paper cited above.
4. Nash, L. G., Phillips, M. N., Nicholson, H., Barnett, R., & Zhang, M. (2004). Skin ligaments: Clinical Anatomy, 17(4), 287–293.doi:10.1002/ca.10203 
Foster, E., Wildner, H., Tudeau, L., Haueter, S., Ralvenius, W. T., Jegen, M., … Zeilhofer, H. U. (2015). Targeted Ablation, Silencing, and Activation Establish Glycinergic Dorsal Horn Neurons as Key Components of a Spinal Gate for Pain and Itch. Neuron, 85(6), 1289–1304.doi:10.1016/j.neuron.2015.02.028