Friday, June 29, 2007

Skin and Autonomics

In PT manual therapy there seems to be some sort of horrified embarrassed mental block about the info I'm going to place here in this blog, as if wanting to understand these kinds of mechanisms was equivalent to wanting to wander into church completely naked. In the interests of deconstructing attitudes that make absolutely no sense to me, I've decided to share this info here.

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.

Monday, June 18, 2007

The Problem with OMPT: Part II

The following is something I wrote this morning in the MyPTSpace pain forum in an attempt (which may be in vain) to clarify what I'm wanting to show by doing a study on DNM:
I'm not sure why you think pain patients are a different group than regular patients. Do not all patients who arrive for PT treatment have pain, or at least discomfort when they move parts of their body? Is that not why they come in the first place? Seems to me that all PT outpatients have at least three things:
1. Intact functioning nervous systems, i.e., no major neuro deficit
2. Skin, usually intact and also functional
3. Pain of some kind.

They may or may not have some kind of mesodermal joint/bone/muscle problem. We just don't know. Even if they do it may or may not have anything to do with the discomfort they feel. These are correlations, and we may not assume cause if we are serious about being clinical scientists. Yes we've been "trained" to treat as if cause were to be assumed, but in fact, "education" tells us we can't get away with that if we are going to start sorting our profession out a bit more logically.

So, what do we do with all these people coming in to see us that may or may not have a mesoderm issue but who almost 100% of the time have a pain complaint? Well, why not devise a way to lower the pain factor *first*? Then, all the patients for whom the pain was causing the "impaired" function, will separate themselves out into a beautiful and identifiable "subgroup", leaving those whose pain may be lessened but who still have a *mesodermal* impairment of some sort, in another beautiful and identifiable subgroup, who then can go on to be treated in the myriad of ways that will benefit *them*. And less painfully to boot.

See, really I'm trying to make our professional lives easier, not harder. I really would like to see how well the horse could pull the cart instead of forever plodding along behind it. My study will be a test of how well horses can pull carts. I'd like to see DNM and by extension all "ectodermal" therapies, become a simple and effective sorting tool for the profession to use.

Don't worry, the profession will always need the mesodermal people too. Cows are animals but surely not all animals have to be cows.

Bear in mind I am not diagnosing and treating impairments. I am not stretching an area of skin because it is tight and then saying treatment will probably be successful because the skin there isn't tight anymore (this is essentially what the MFRers are saying about fascia for example). If I were, then arguments about the reliablilty and validity of diagnostic testing and outcome would be appropriate.

But all I'm saying is that novel, skin-based input at and surrounding the symptomatic region may modulate ongoing nociceptive processing. While this certainly requires construct and face validity (which, while not yet 100% proven, I think I am in the process of addressing satisfactorily), it does not require reliable methods of finding impairments that I'm not treating anyway.

So the only real question is what essential diagnoses is this method appropriate and effective for. And since we really have no reliable clinical methods of determining essential diagnoses for most pain conditions I say we need some basic research here, which I will do, to see if DNM is as good or better than other methods that are really no more certain, as a sorting tool to see which patients or what percentage or kind may *need* a stronger form of manual treatment and which ones most definitely do not.

In retrospect, I'm sure they'll jump all over me for having used the no-no word "all" in the first paragraph. I should have painstakingly qualified that by using the word "most" or "virtually" as in "virtually all".

Sunday, June 17, 2007

"The Problem with OMPT"

I just love this post that appeared this morning, simultaneously in two places; one place was SomaSimple (where the link goes), and the other is Evidence in Motion, a PT site where a few "defenders of the faith" soldier on to try to maintain the argument that orthopaedic manual therapy is the best PT has to offer the nation (U.S.) and therefore the world.. It was written by a DPT who is also an U.S. army captain stationed in Germany. He happens to be a very clear-thinking individual who is not still involved in some protracted honeymoon bliss with manipulation.

All this sits on the top of an intense debate that has raged for months on EIM, deep in its bowels, deep in the MyPTSpace community forum that supposedly has to do with discussions of pain. Almost as soon as the community formed, and some PTs (including me) went on there to discuss.. um, pain, we were subject to all sorts of barking and yipping at our virtual heels by a couple members who see our presence there as a threat to themselves somehow. One of them even said just yesterday he wished he could reach through the computer to "wring my neck". It's the first time I've been actively threatened, in my life, by someone who is a complete stranger (other than knowing him through volleys of posts), and who calls himself a PT. I've either led a charmed life until now or he was just kidding, and hit "reply" before editing. Once you post there, no editing is possible. So I will give him the benefit of the doubt. Furthermore, I see no point in reacting particularly to a mere virtual threat - he's a long way from me geographically. Besides, the feeling's somewhat mutual... and I know (using my mirror neurons) I'd never act on such a feeling. It seems to me that's what science is for, to settle disputes, especially ones that lend themselves to scientific solutions.

Speaking of science, what made him so mad was that I began to discuss a new project that Angela and I might just take on in the future (dreaming is still free, right?), that would set up an RCT with three arms, one arm that is a control group, one that treats according to the usual ortho standards, and the third arm me.

Now you might read this and think ok, that sounds interesting, or ok, that sounds boring, but to this individual and to a few others, it sounds threatening. They are not scientifically mature enough to welcome challenges to the world as they know it, especially to their mesodermal treatment constructs.

Enter Jason's post. It has dampened down the forum a bit. For awhile. It would seem. Which is good. Very good.