Earlier in the spring someone said that I couldn't state anything about handling skin being able to affect autonomics in the skin in the newsletter piece I submitted. Six weeks after, I had a bit of time, dug for this basic info and sent it to him post publication. So here is what I found out, a bit more support for treatment of cutis/subcutis having something to do with autonomic function/change. I hope no one thinks any of this info is "crazy". It's basic research out of Australia, done over the last 20 years or so.
1. From p. 133 of the Autonomics of Skin, a book in the Geoffrey Burnstock series, Chapter 5, "Autonomic Control of Cutaneous Veins", by Loring B. Rowell:
"Veins of the skin in many mammals form a capacious network - even in those not experiencing the great increases in cutaneous blood flow seen in humans. We are unique among mammals, especially those who bear fur and must pant to exchange heat. Some mammals have powerful vasodilator and heat exchange mechanisms in the dense vascular network of the tongue where blood is evaporatively cooled. Others have specialized vascular networks such as the carotid rete that provide counter-current exchange of heat between arteries supplying the brain and veins draining cooler tissues. These structures permit separate cooling of the brain without at the same time requiring decrements in temperatures over the rest of the body. Unlike these mammals, humans have no significant heat-exchange mechanisms in the head that can minimize the rise in brain temperature when body temperature rises. Therefore we must cool the brain by cooling the rest of the body."
Right here, we see that human skin is special. It needs to breathe, and be cool. Add to this the fact that our brain is 5 times larger than needed to operate a mammal our size, and you've got to think, is it any wonder we lost our fur? We had to or our brains would have probably overheated. We are the sweating mammal.
2. "In humans the entire burden of cooling the central nervous system during heat stress falls on sweating and the cutaneous circulation (Rowell 1986). This means that brain and body temperatures are controlled together as a single unit. Most of our heat exchange occurs within a dense system of capillary loops and the capacious subpapillary venous plexus into which they drain. Human skin is unique in its vascular anatomy, the density of its vascular supply, and the innervation of its arterioles, which contain a powerful active vasodilator system. These features fit with its uniquely important role in temperature regulation (Rowell 1974a). Innervation and control of the cutaneous veins appear to be similar among species, but only in humans does the cutaneous venous system receive such high blood flows or contain so much blood volume during hyperthermia. The rich sympathetic innervation of cutaneous veins permits them to actively constrict, thereby conserving body heat during cold exposure. Their constriction diverts venous return away from the body surface to deep veins that are not constricted, establishing what is in effect a "thermal short circuit"."
The sympathetics have to do everything - i.e., there are no parasympathetic outflows to skin. Sympathetics control both the ebb and the flow out there in the skin layer, an ebb and flow unique to humans apparently.
3. Chapter 6 , "Cutaneous Effectors as Indicators of Abnormal Sympathetic Function" by Phillip A. Low (who went to school in Aus) and William R Kennedy, both of whom work in the U.S. From p 166:
"Skin sensation for touch, temperature, and pain exerts a strong influence upon sympathetic nerve activity."
There it is in black and white. Touch affects autonomics.
4. "The location of the nerve endings that convey these modalities has recently been put into question with redescription of the innervation of epidermis by a complex of unmyelinated nerve fibres (Wang et al. 1990; Kennedy and Wendelschafer Crabb, 1993) that are not included in sensation theory (Light an Perl 1984). Although epidermal nerve fibres are almost certainly sensory, they may have motor-like influence on their environment through secretion of neuropeptides (Eedy 1993; see Holzer, Ch. 7 this volume)."
So, sensory fibres (which are actually long dendrites according to Larry Swanson who wrote "Brain Architecture") can operate as axons too, autonomic axons.
5. "There is an intimate relationship between skin blood flow and pain in several disorders. Skin blood flow reflects vasomotor tone which is determined by the level of sympathetic activity. The relationship between sympathetic activity and pain has recently been reviewed (Jänig and Koltzenburg 1991)."
Apart from the fact that the author uses the word "pain" (a neural output) instead of the word "nociception" (a neural input), a common error still committed by way too many writers, this makes complete sense.
6. In chapter 7, by Peter Holzer, page 214:
"Under appropriate circumstances...primary afferent nerve fibres can behave AS IF they were axons of autonomic neurons. We now know that afferent nerve-mediated control of vascular functions is due to the release of vasoactive peptide transmitters from the peripheral fibres of fine afferent neurons."
More about sensory fibres being two-way streets.
My bolds. I suspect this is at least part of the mechanism by which physiological changes can occur in a patient with little or no physical effort on the part of the therapist, no biomechanical obsession, no need for strenuous evaluation, no need for painful provocation testing, maybe little or no need for the entire orthopaedic slant of Manual Physical Therapy (said with hope that OMPTs can find some way to forgive me some day). Self-correcting mechanisms within the nervous system itself, elicited with only a modest amount of the right sort of mostly non-nociceptive input. A prerequisite is rapport with the patient, but only enough for them to be able to accept handling from the therapist. No need to ever go into deep emotional baggage or bonding or spiritual realms. Bio-logical. (Physical) Therapist as catalyst, nothing more. Facilitate some change in the chemistry a little in the periphery, combined with S1 neuroplastic changes, assume the brain is reading it all like crazy, that a small amount of sustained input over a longer period of time will make its way quickly around the system, hang out long enough to perceive a change in the system's output, then move on.