Narrow Trail Walking

In this age of reduced car use I've developed a personal practice/ treatment strategy/ homework piece that I call "Narrow Trail Walking". It involves walking at a normal pace, with a normal length stride, but with one foot directly in front of the other as if one were walking on a narrow trail. Feet are to be kept pointing forward.

We become awfully lazy walkers on our smooth, sprawling sidewalks. Most people walk as if they were on a trail about a foot wide; I ask them to practice walking on one that is just one foot-width wide. At first people walk as if they were walking a plank (all tentative, slow, eyes to the ground, arms out to the side for balance) and need to be reminded that they're still on the flat ground, won't fall, to just stride along.

To stride requires elongation of forward leg and telescoping or shortening up into the body of the back leg. Of course, all this is handled by the pelvis and low back, not the legs themselves, but it's a useful sensory cue to give a patient at first. Once they've got the rhythm, then one can tell them to become aware of how the pelvis has to rock and roll to get the legs smoothly organized, how the back has to sidebend/shorten on one side, while elongating on the other. Both lumbosacral plexuses get flossed alternately.

Next, I ask them to become aware of how their trunk must be capable of twisting and "wringing" to remain facing forward. This is a bit of a "stretch" for most people accustomed to walking like robots, with no trunk motion whatsoever.

The next piece is the arm swing. Invariably people try to swing the same side arm and leg at first, but they correct it easily once they know to, alternate to the legs which are going along fine by now. Voilá, all the peripheral nerves are now flossing through the body from the neck down. The spinal cord is rotating/wringing like a non-rigid bidirectional washing machine agitator, flexing and elongating, feeding itself inside its columnar support with every step.

The last piece is to ask them to keep their eyes level on the horizon, looking for food/predators, like any proper biped. It's interesting how fast heads stop bobbing. The neck automatically starts to do what it's supposed to do, i.e., adapt to movement from below, and balance a still head effortlessly over a moving body.

This N. American culture does not model simple walking very well to its children. I started imitating runway models, but they prance too much. So I kept the crossover portion but toned down the prance, then realized I was walking the way we bipeds likely evolved, on little trails through long grass, every cubic inch of body generating or receiving some sort of motion in the process. My kinesthetic input conjured up visual images of every example of truly graceful walking I'd ever seen. After awhile it does feel effortless and natural, and one needn't be a woman to walk gracefully. Narrow trail walking can take care of lower limb pain to a large extent, and keeps the outside of the legs stretchy and extensible.

"Go Animal"

I've placed a link to this site in the link menu to the right. I found this site quite by chance one day while googling info on long term potentiation.

Frank Forencich is a combination physical educator, neuro science lover and author. His newsletters are a delight to read, although sadly he seems to write them quite rarely. I guess he's out doing what he loves, which is moving.

"Sicko"

I went and saw this movie last night. It had some shocking, several touching, and many hilarious moments, all the better to convey the main point, i.e., the absurdity of the U.S. healthcare system's provision of health care BY bottom line profiteers.

In one scene, Michael Moore is sitting at a table of American ex-pats in France, sipping wine with them while they tell of the ease with which they raise their families in a family centered place like France. The government supports child-rearing by providing heavily-subsidized, universal daycare and even nanny-support. When the spectre of high taxes for such exquisite provision is raised for discussion, we see into a typical middle class French home complete with children, decorated with original art and souvenirs of trips abroad, taken with the 5 weeks of (paid) holidays commonly enjoyed for family bonding time. The homeowners state that holidays are probably their biggest household "expense".

At the table of ex-pats, Michael Moore can't take it anymore, sticks his fingers in his ears and sings "La-la-la-la...."

A touching moment (for me) was his interview with a Canadian on a golf course, who although he identified himself as a Conservative, wouldn't dream of trying to change the Canadian health care system as was envisioned by T.C. Douglas.

The movie captures all the blank looks of disbelief and smiles on the faces of citizens of non-US countries as Moore probes them for the political dirt - surely there must be a catch, right? After all, the powers-that-be in the US talk about all the terrible conditions that exist in socialized medicine countries, so they must be hiding the real truth, right? What is the true "cost" of all this "free" care? Try as he might, he just can't seem to find any smut to highlight. People seem happy, secure, peaceful, and in control of their lives. Governments in charge of operating egalitarian health care systems exist to carry out the "will" of the "people" to have the right to ...normal existence; happy, peaceful, secure and in control of their personal lives. Not the other way round.

By contrast, in the U.S., people, even those who can afford the $600 or so per month insurance premiums, have no guarantee they will be covered. A man who used to work for a health insurance company is interviewed - his job once was to screen out people as ineligible AFTER they received a medical diagnosis or treatment. They are rewarded for saving the company money by denying claims.

What if a patient has no insurance? They can end up dumped by a cab in front of a homeless shelter in the middle of the night, still wearing a hospital gown.

TakeHome Points about Autonomics to Skin

Here is a section of the concluding remarks Gibbins makes towards the end of his chapter, my bolds.

Quote:

GENERAL FEATURES OF AUTONOMIC PATHWAYS TO CUTANEOUS EFFECTORS

From the preceding account, it is obvious that the skin is a major target of the autonomic nervous system in most vertebrate groups. In mammals with hairy skin, up to 25% of neurons in the paravertebral sympathetic ganglia lie in pilomotor pathways in addition to various populations of vasomotor neurons. Although few details are known, there is likely to be at least as large a pool of neurons supplying the dense innervation to the sophisticated pennamotor system of birds. Mammals with extensively innervated and widely distributed sweat glands, such as humans, have up to another 15-25% of their paravertebral sympathetic neurons in sudomotor pathways. Similarly, 25-50% of neurons in the sympathetic ganglia of anuran amphibians lie in cutaneous secretomotor pathways. Overall the skin represents a substantial target of the autonomic outflows, rivaled in size and number of neurons only by the sympathetic vasoconstrictor pathways that supply virtually all of the vasculature in most vertebrate species.

Despite significant and marked differences in the details of the cutaneous autonomic pathways, some common features are apparent. Most obvious of these is that the final motor neurons in the cutaneous pathways tend to run out to the skin in a segmental fashion, travelling with the sensory fibres in cutaneous branches of the spinal nerves to the dermatomes. The autonomic dermatomes usually are not as well defined as the sensory ones, but they have the potential to allow a unique insight into the organization of peripheral autonomic function. This characteristic has been utilized well in studies of the control of colour change in teleost fish and in abnormalities of sweating function in humans.

The final motor neurons in cutaneous pathways show surprisingly constant differences in the pathway-specific expression of their morphology and neurochemistry (Figure 1.11). In all species examined to date, neurons in vasoconstrictor pathways have the smallest cell bodies. Moreover the smallest of the vasoconstrictor neurons are those projecting to cutaneous vascular beds. As in the case elsewhere in the nervous system, it is generally accepted that the size of a sympathetic motor neuron and the complexity of its dendritic arborisation is related to the number of synaptic inputs it receives. It is likely therefore, that cutaneous vasoconstrictor neurons receive less synaptic input than do pilomotor neurons in mammals or cutaneous secretomotor neurons in frogs. The size of neurons cutaneous vasoconstrictor neurons generally have slower conduction speeds than autonomic motor neurons in other cutaneous pathways. Why this should be so is not clear. However, one potentially important factor is that the vasoconstrictor pathways tend to be tonically active, whereas the pilomotor and secretomotor pathways tend to be activated only in specific circumstances. Synaptic transmission in vasoconstrictor pathways tends to be very reliable, often requiring only one suprathreshold preganglionic input. In contrast, it might be predicted that the larger pilomotor and secretomotor neurons are only activated after summation of several preganglionic inputs. This prediction remains to be tested.

The neurochemical differences between different functional classes of neurons in cutaneous autonomic pathways provides unambiguous evidence for the presence of highly specific pools of neurons projecting to well defined effectors. Within the cutaneous vasculature it is clear that there are separate populations of neurons projecting to the proximal vessels, small distal vessels and AVAs and veins. It is also clear that pilomotor neurons form a well-defined population distinct from any of the vasomotor neurons. Furthermore, it is likely that cutaneous vasodilator neurons, when present, are distinct from sudomotor neurons. These results are consistent with more recent studies on the central pathways responsible for autonomic activity which indicate that there is a series of distinct areas in the periaquaductal grey, hypothalamus, and medulla that activate specific autonomic pathways in response to well defined changes in the external or internal environment. Furthermore, it is clear from physiological and anatomical studies that there are separate pools of preganglionic neurons projecting to different functional population of cutaneous motor neurons. Although we still do not know how the central areas are connected to the final autonomic motor and premotor neurons responsible for generating the appropriate effector activity, it is absolutely clear that there is no such thing as a generalized autonomic outflow, and that the widespread activation of different cutaneous effectors must require the coordinated recruitment of multiple independent autonomic motor pathways.

Piloerection

From Ian Gibbins' excellent book chapter (Ch. 1 in Autonomic Innervation of the Skin, 1997) on autonomics, p. 29:

Pilomotor neurons also can be distinguished from most vasoconstrictor neurons by the size of their cell bodies and dendritic arborizations. Thus the pilomotor neurons, on average, are larger than vasoconstrictor neurons in mice and guinea-pigs (Figure 1.6; Gibbins 1991; Gibbins and Matthew 1996). This result is consistent with physiological observations in cats showing that pilomotor neurons generally have faster axon potential conduction velocities than do cutaneous vasoconstrictor neurons (Jänig 1985). The reasons for these differences are not clear, but two points are worth considering in this context:

1. Sympathetic final motor neurons with larger dendritic arborizations tend to have more convergent preganglionic inputs than neurons with smaller arborizations (Purves 1988). Thus, in general, we would expect pilomotor neurons to receive more preganglionic inputs than vasoconstrictor neurons.

2. Sympathetic final motor neurons within pathways that are used only intermittently tend to be larger and have faster action potential conduction velocities than those that are tonically active. Thus within the superior cervical ganglion, for example, cutaneous vasoconstrictor neurons, which are active most of the time, are smaller than pilomotor neurons, which are themselves smaller than salivary secretomotor neurons which probably are activated only rarely.

Most of the information on the organization of pilomotor pathways comes from studies in cats (Langley and Sherrington 1891; Langley 1894; van Rijnberk 1907; Jänig 1985; see also Lichtman et al. 1979 for a study on guinea-pigs). Mostly the pathways that have been studied are those activated during the fear/aggression response. In cats under these conditions, piloerector activity occurs in the facial skin between the eye and ear, a strip about 10 to 12 cm wide extending from the back of the head along the dorsal midline to the base of the tail, and most of the dorsal and lateral part of the tail (Langley and Sherrington 1891; van Rijnberk 1907; Jänig 1985). Although pilomotor muscles themselves are more widely spread than this within cat skin and seem to be innervated, the conditions under which they are normally activated are not really know: presumably they have a role in thermoregulation, but surprisingly, this has not been show explicitly. Certainly, in other species such as rodents (guinea-pigs, rats, mice) and primates (rhesus monkey, human), cold-induced activation of piloerection is widespread over much of the skin.

I have to stop for a moment and consider that strip of skin down the back of the cat that stands the hair up in a fear/aggression display. Just because it is so visible in cats, does this not happen with many animals? I recall a Siamese fighting fish I once kept, who did this upon seeing his own reflection in a glass, every time.

Does this not happen with humans? Is not "get your back up" a common expression? I can often feel a "shudder" and other weird sensations shoot down my back, and wonder if these are related in any way. Pure speculation, I realize..

Dorsal cutaneous nerves innervate that particular strip of skin. I see an implication: could it possibly be, that the sympathetic neurons ... that innervate piloerector muscles in skin... skin which is supplied by dorsal cutaneous nerves... have a closer relationship with the bits of brain that have old mammalian (pre-mammalian even) sympathetic fight/flight reactions?

It makes me wonder about any possible relationship there might be among circulating stress hormones, need to suppress aggression/display submission within our human primate troop (i.e., get along),.. to chronic back pain. However tenuous.

I visualize the cutis/subcutis smooth muscle cells along the spine, a spinal "Mohawk" of smooth muscle lifting with all its might, but alas, barely any hair to lift and struggling all the while against clothing and chair backs, piloerecting like crazy but nothing visible to show for it. Us, barely aware of their efforts to express themselves/our non-conscious responses. Us, completely involved in our conscious, inhibiting, troop-appeasing, socially appropriate descending control of muscular effort to provide deceptive "cover".

Could it be that a "war" between brain modules is constantly raging? Expressed by smooth muscle cells (tiny), against somatic muscles, much bigger and more under conscious control. Dorsal cutaneous nerve rootlets pulled this way and that, and secreting like crazy, all the stress stuff that gives them the neural equivalent of diaper rash (abnormal impulse generating sites) inside their little neural cages - I mean tunnels. Especially in those human primates who are lower ranking in the human primate troop. Having to put up with horrible bossy bosses or just life as a worker in general. Having to fake being cheery even if they don't feel it. Low back pain for no "good" reason, such as a definitive injury, an all too common human fact of human life.

Anyway, just some idle speculation on my part. What else is a blog good for?

The pilomotor pathways have an overall segmental distribution, that loosely follows the sensory dermatomes, especially on the trunk (Langley 12894; van Rijnberk 1907; Jänig 1985). For much of the body, the preganglionic fibres in pilomotor pathways project directly from each spinal segment to the corresponding ganglion; i.e., they do not project up or down the sympathetic chain to a significant degree before connecting with the pilomotor neurons themselves. Similarly the pilomotor neurons project directly from their ganglion into the corresponding spinal nerve. Overall the preganglionic neurons in pilomotor pathways of cats extend from spinal segments T4 to L3 or L4 (Langley 1894). The pilomotor neurons innervating the skin of the head arise from cell bodies in the superior cervical ganglion and receive inputs from preganglionic neurons in upper to mid thoracic level spinal segments (T4 to T6 or rarely T7 in cats, T4 to T6 in dogs, Langley 1894; T1 (rarely) or T2 to T5 in guinea-pigs, Lichtman et al. 1979). In guinea-pigs there is a clear correlation between the level of spinal origin of the preganglionic neurons and the region of skin innervated by pilomotor neurons. Thus, neurons with preganglionic inputs from more rostral spinal levels tend to innervate piloerector muscles on the more rostral and ventral areas of the face whereas neurons with preganglionic inputs from more caudal segments of the spinal cord tend to innervate piloerector muscles on the more caudal and dorsal regions of the head (Lichtman et al 1979).

The central pathways generating piloerector responses clearly must include areas of the hypothalamus associated with thermal regulation, such as the preoptic/anterior hypothalamus, and areas such as the amygdala and the periaquaductal grey involved in generating aggressive or defensive behavioral displays (Schönung et al. 1971; Swanson and Sawchenko 1983; Smith and DeVito 1984; Hilton and Redfern 1986; Holstege 1990; Jordan 1990; Gordon 1993). In particular stimulation of the lateral areas of the periaquaductal grey can cause piloerection as a component of a induced threat display in cats (Bandler, Carrive and Zhang 1991). Although all these areas are known to project directly or indirectly to the spinal cord (see Holstege 1990; Swanson 1991), nothing is known of the specific pathways linking these central areas to preganglionic pilomotor neurons in the spinal cord.

Periaquaductal grey areas are part of the fish brain (basal ganglia) as I recall.. I can hardly wait until people like Gibbins get the pathways more sorted out. I think the implications are quite big, actually.

Steven Rose, Future of the Brain, excerpts

I love his action verbs - he uses them in such a way that it creates a clear mental movie to watch. From p. 72:
Quote:

Young neurons must recognize their migratory path and move along it; finally they must at some point recognize when to stop migrating and instead begin to aggregate with other neurons of the same kind, put out axons and dendrites, and make the right synaptic connections... As the glia migrate they spin out long tails up which the neurons can in due course climb. The cell membranes of both neurons and glia contain a particular class of proteins called CAMs (cell adhesion molecules). In the developing tissue the CAM work a bit like crampons; they stick out from the surface of the membrane and cling to the matching CAM on a nearby cell; thus the neurons can clutch the glia and ratchet themselves along. As a further trick the migrating cells also lay down a sort of slime trail of molecules related to the CAMs - substrate adhesion molecules or SAMs - which provide additional guidance for the cells following. The neurons can move along the SAM trail rather like amoeba - that is, they ooze.

This part is reminiscent of Into the Cool, "Nature abhors a gradient" :
Quote:

What provides such map-references for the cellular route-marches? Even if neurons follow glia, the glia themselves must have a sense of direction. Both distant and local signals must be involved. One way of signalling direction is to have already in place some target cell or tissue towards which the migration must be directed. Suppose the target is constantly secreting a signaling molecule, which then diffuses away from it. This will create a concentration gradient, highest at the target and progressively weaker at increasing distances from it, just as in the case of the unicells discussed in the last chapter... early born neurons secret a protein called reelin which sticks to the molecular matrix surrounding them, acting as a stop signal for each wave of arriving cortical neurons, telling them to get off the glial fibre and develop into a layer of mature neurons.

He uses principles established from other orders of magnitude to illustrate more about brain development, e.g., survival of, if not the fittest in a reproductive sense, survival of the fittest in terms of those most adept at connecting:
Quote:

..there is a further process operating here. During embryonic development there is a vast overproduction of cells. Many more neurons are born than subsequently survive. More axons arrive at their destination than there are target cells to receive them. They must therefore compete for targets. Those that do not find them wither away and die. There is this in this model of development, competition for scarce resource - trophic factor, target cell, synaptic space.

He goes on to be more explicit:
Quote:

This overproduction of neurons and synapses might seem wasteful. It has led to the argument that just as during evolution 'natural selection' will eliminate less-fit organisms, so some similar process of selection occurs within the developing brain - a process that the immunologist and theorist of human consciousness Gerald Edelman has called 'neural Darwinism'. However, this transference of the 'survival of the fittest' metaphor from organisms to cells is only partially correct. It seems probable that the whole process of cellular migration over large distances, the creation of long-range order, requires the working out of some internal programs of both individual cells and the collectivity of cells acting in concert. Even though synapses from only a particular neuron may end up making successful connections with its target cell, if the others had not been present during the long period of growth and migration it is doubtful whether a single nerve axon would have been able to reach the target. Survival of one depends on the presence of the many. Overproduction and subsequent pruning of neurons and synapses may at one level look like competition and selection; viewed on the larger scale, they appear as co-operative processes. It seems to be necessary, to ensure that enough cells arrive at their destination and make the relevant connections, that others must assist them, only themselves to die en route - a process called programmed cell death or apoptosis. Indeed, in a creature like C. elegans, ... those neurons destined to be born and to die en route to their seemingly final destination can be identified from the start. The process is orderly rather than random.

Here is something that is dear to me, because I thought of it independently - the idea of environments within and not just without. This makes total sense to me who sees the body as an ecosystem, kaleidoscopically, from multiple viewpoints, from the viewpoint of every cell (p. 59):
Quote:

'The environment' is as much a myth as is 'the gene'. Environments exist at multiple levels. Thus for an individual piece of DNA 'the environment' is all the rest of the DNA in the genome, plus the cellular metabolic system that surrounds it, proteins, enzymes, ions, water ... For a cell in a multicellular organism... the environment, constant or not, is the internal milieu in which it is embedded or adjacent cells, signalling molecules, bloodstream and extracellular fluids. For organisms, the environment is constituted by the biological and physical world in which they move...

This supports the idea that the environment of nerves is just as important to them as the environment around anyone is to anyone.

There are more delicious bits in this book, but what I most appreciate so far about Rose is how he sees the human organism and all subparts of it and all functions of them as verbs, not nouns.

Podcasts About the Brain

These are great. Check them out. I've linked to a list of all of them, and to Dr. Ginger Campbell's discussion forum. (There is also a link to the discussion forum on the right, in the link menu.)

The Future of the Brain, by Steven Rose

I'm departing briefly from the topic of autonomics to mention that this book is great. The first couple dozen pages on evolution (in the beginning of Chapter 2) are alone worth the price of the book - everything from how single cells do things, to a brief discussion of symbiogenesis, to limitations on size, an evolutionary process called exaptation, and "homeodynamics" (which he suggests is an improvement on the term "homeostasis") then he starts to discuss the evolution of the brain itself.

Are we "sympathetic" enough?

From p. 10 of Autonomic Innervation of Skin (1997), Chapter 1, Cutaneous Autonomic Pathways, written by Ian L. Gibbins:

"..most of the autonomic vasodilator innervation of the face of normal humans is of sympathetic origin with nerve cell bodies probably located in the superior cervical and stellate ganglia. However, there is also likely to be a parasympathetic vasodilator innervation to specific regions of the facial musculature, particularly that of the lips and forehead. This pathway can be activated by noxious stimulation of the eye or oro-nasal cavity (Drummond 1993, 1994; Kemppainen et al 1994). In some cases, it accompanies eating. This vasodilator response usually is accompanied by sweating, hence the term "gustatory sweating" that sometimes is used to describe this phenomenon (see below). These responses survive sympathetic blockade, and even may be enhanced after chronic loss of sympathetic activity. They probably are due to activation of facial nerve and glossopharyngeal nerve pathways (Drummond 1994), presumably homologous to those described above in rats and cats, via sensory pathways running in the trigeminal nerve."

I was surprised to learn, a number of years ago, that there was no parasympathetic innervation to skin in humans. One of those myths I swallowed pretty much whole way back when, a blithe assumption adopted by soft tissue manual therapy types like myself, was that there was some sort of global parasympathetic response by the human organism to hands-on work, in other words, via skin input. I mean, there had to be, right? People relaxed, and their tummies gurgled; that meant a parasympathetic response, so there must be parasympathetic nerves in the periphery, in the skin, right? Didn't blood vessels dilate? Wasn't dilation "caused" by parasympathetics?

Wrong.

This idea was actively fed as a treatment hypothesis, and/or never properly countered by purveyors of the courses that taught the hands-on work. The same individuals seemed to never carefully check and/or even list their sources. They continued to thereby allow ignorance to slow down the speed of understanding this form of human primate social grooming from a scientific perspective. Only much later did I come to understand, as an individual practitioner, that some kind of global parasympathetic response to direct touch or handling was frankly impossible, that everything out in the body that can be touched, including skin over those forehead and lip muscle bits, is sympathetically innervated, and will react sympathetically.

This only makes sense, given that parasympathetics are mostly about digesting (we don't digest on the outside.. we don't take food in through a surrounding membrane anymore as single cell creatures do). Given our skin is the first layer of sensory protection against exteroception and primarily a radiator for cooling the brain, it especially makes sense given that sympathetics do everything, vasoconstriction or dilation, depending on how they hook up, what transmitters they respond to, and what sort of size they are.

But what about that gurgling? In view of the fact that the brain is not monolithic, that in fact we could even say it's still full of all the creatures we once evolved away from (see "The Beast Within") and knowing that there is no parasympathetic innervation to skin, we could instead conceptualize that some sort of inner highlighting of non-conscious threat tension ensues, and is successfully resolved, right inside the system with which we are engaged. Butler is fond of saying, "Remember, just as you are reading a patient's nervous system, theirs is reading yours." The skin and sensory motor part of the system will see exteroception as a "threat", no matter how kindly it is provided. The human/primate/mammal level probably will not. There will be a battle of sorts within that system, completely invisible from the outside but palpable. The "higher" centers will prevail by regaining the ability to do what they do best, which is inhibit, and peace will be restored to both the body and to the individual who can now more comfortably inhabit that body. If we as practitioners think that we have anything more to do with this process other than catalyze it with handling, we are full of it. The patient's brain does it all, and then gives us some credit (probably ill-deserved much or even most of the time).

Back to the point, about good info on sympathetic/parasympathetic innervation or lack thereof, looking back, I have had more than a few moments of irritation, realizing that it's actually a very deep insult to be treated as if one were nothing but a pair of hands to be trained, no real care taken about what goes into the cognitive "compost bin" attached. Furthermore, I have a lot of irritation that I let my own personal cognitive compost bin be filled with meme garbage of varying kinds, some good and a lot bad. I've done a lot of subsequent composting, finding and tossing out incongruent bits of info; like small toy trucks, they don't break down or blend in, so they are easy to spot and remove. I've turned and aerated the contents on a regular basis, but mental composting is never really finished. It's always a work in progress; eventually however, you can extract something that looks like fertile soil, something that looks like it could sustain mental growth.

More important even than what goes in the bin is how the bin is constructed in the first place - one wants a bin that is rat proof. Instructors who name reliable external sources give one the means with which to reinforce the bin anywhere/everywhere, anytime. I can say without hesitation, don't ever waste your money going to courses where no one names sources, or where the sources are only vague or self-referent. The maintenance of a solid bin is too important in the long run, and developing gentle means by which to handle people in pain is too strategic a goal to permit its continued erosion by poor scholarship.

How does one correct the direction soft tissue work took way back when? One can't - one can only save oneself, share the story, warn others, and demand higher standards in general.

Autonomics, Skin, and Sensory Input (Exteroception)

The title of this entry is linked to a thread I've been working on at SomaSimple lately, on this particular topic to which I think the entire world of human primate social grooming should expose its group mind.

Of particular interest to me this morning is this little tidbit, from the preface of Autonomic Innervation of Skin and to all (I think) 14 volumes of the Burnstock series:

...the concept of antidromic impulses in sensory nerve collaterals forming part of 'axon reflex' vasodilation of skin vessels was described many years ago (Lewis, 1927).

What? 1927? TWENTY-SEVEN ??

Most of our professional existence has been after that particular date. Why wasn't this little factoid hammered into our receptive PT brains from day one, I'd like to know? We who are charged with handling people all day/every day?

Autonomics in skin

I have been thinking a lot about that last post, about sensory fibres behaving like two way streets, able to operate as autonomic motor (E-ffector, output) fibres as well as sensory (A-ffector, exteroceptive input) fibres.

I really, truly think this is a key piece for us as PT manual therapists.
I really, truly think this is a key piece of info that has been until now (pick one or more from following list):

1. never learned properly or explicitly
2. never understood within a frame of how touch can lead to physiological changes
3. bypassed as "too hard" or insignificant
4. not taught
5. taught but not emphasized
6. never linked to anything manual, never linked to any manual technique class
7. never taken seriously by our profession, or else our "as-if" capacity was never permitted awareness of even the slightest possibility that something like this could be remotely true
8. unavailable to a profession that prides itself on being science-based because it has only recently been verified/verifiable.
9. not allowed to inform our treatment constructs

There are probably more ramifications/ extrapolations I haven't thought of yet to put on this list. But for now, I'm just living with this info as if it were a new lens through which to view the entire world of manual therapy.
Mind-boggling to me, the infinity of how this little piece of basic info could change everything about everything... provided we were to let it sink all the way in.