Kinesthetic Conversation

[Diane]

Nature never throws out anything that "works". If we accept the idea that evolution occurred and that humans are no longer the same vertebrates that fish started out as many million years ago - we might also accept the idea that the nervous system we own and operate is a modular system, like an old farmhouse that was never torn down but was instead just added on to, as new needs arose.

Somehow all these "parts" to our nervous system accumulated leaving us with what we have to deal with today. They have to get along somehow. We are verbal creatures and think in pictures or images, but the parts of the nervous system that run our bodies (http://www.somasimple.com/forums/showthread.php?t=4170) do not - instead they work completely non-verbally, non-consciously, by producing body states, about which we develop sets of "feelings" once we realize, once we become aware that our heart is pounding, etc.

When we treat the "body", really we are treating the entire nervous system through this very old, very primitive part of it. It does not speak. It acts. It tries to get away (http://www.somasimple.com/forums/showthread.php?t=3871&highlight=letting+the+nervous+system).

Of course, it can't get away because it's embedded in a "body" that it has no awareness of - it's job is to keep the body oxygenated... and in the process, keep itself/its own PNS oxygenated.

So, what can we do to engage this portion of the nervous system? It can't "see", except through human filters. So having the eyes closed is a good idea. This sharpens kinesthetic sensing. Oxygenation is an important task for this part, so giving IT a rest by taking over breathing, consciously, makes sense. It is constantly trying to move, so tuning in to find that movement and letting it happen, is a good idea.

As therapists we can engage it in a patient, by contacting skin. A lot of the fish brain exists in the cutis/subcutis layer, a very handy arrangement that we can take full advantage of. By putting our hands on someone we are inviting their nervous system to "tell" us how it "feels". This is the only theme/topic in a kinesthetic conversation in a therapeutic situation.

Once we have our hands on the skin layer, we can sit still and "fish" - just let our line be in the water until something grabs our our awareness, by kinesthetically stimulating our hands' own massively dense sensory awareness. We can then interact with that movement, "assisting" the local bits of nervous system to escape, moving the skin layer in the same direction that you sense it "wanting" to move.

Bear in mind that other things are happening as well. You might track rise and fall in pain, asking the patient to comment on what they are experiencing in their body. This helps them become more conscious of what the fish brain is trying to do. This movement might feel like anything at all. Several patients have told me it felt like bubbles or fizz to them, and that it was definitely associated with decrease in felt pain. Others see colors flowing through their bodies. It does not matter one bit WHAT they sense or how they image that sensation - what matters is that they can a) feel something, anything, and b) that they explore the sensation without hesitation.

The first is an indication that the human cortex part of the brain can link in to what's going on in the so-called "body" or as I prefer to think of it, fish brain. This is an important skill set to have - people who readily learn to do this will be less likely to develop pain again in the future, because they will be more aware of when their system, body, fish brain needs to move/oxygenate itself. Chances are lower that the nervous system will have to make a big pain production in the future to get their attention. Especially if you take the time to point this out to them.

The second is important in that patients who can fearlessly move their attention around their physicality are, again, less likely to experience pain (bad enough to visit a therapist) again, and also it gives you, the clinician, a chance to observe their ordinary anxiety level. Low anxiety people are more easily treated, for lots of reasons, the main one being (IMO) that they seem to have better stress regulation. High anxiety people seem like they have a really awful time just existing physically in a body in the first place. It's as though their nervous system parts are all terrified - of each other. They don't ordinarily breathe well. They don't seem to feel comfortable with experiencing any sort of sensation from their body, would prefer to block it out of awareness. Their skin may feel waxy and kind of "dead" to you. The person exhibiting these indicators may be simply going through a difficult time in their life, or might be someone who needs to see another sort of therapist.

In a nutshell, kinesthetically conversing can give you lots of information if you let it in. Of course, first you have to be willing to gather your own awareness together, then focus it in your own hands. They need to become not only tools for doing but also satellite dishes for receiving kinesthetic information. In conversations of any sort, it's a good idea to "listen" for longer periods than you "speak".

[emad]

Hi ,

Seems in touch ( communication ) both attention should be ON , which is a state of Attention-on , meaning there is a state of Atenttion-off =Pain but not usually in some instances . I am not satisfied by the history of Brain/attention development which occured in humans history , seems there were long millions incubation periods of attention .

cheers
Emad

[Barrett Dorko]

Diane,

This is a wonderful post and explains so much about what is likely to be sensed and why if we simply focus our attention after reading about what should be happening. Too often, therapists have gone about this backwards.

It's connected to so many other great threads that I can't begin to list all of them, but I think that's because Soma Simple is an emergent phenomenon, and the parts lead to an unexpected but ultimately irresistible whole.

Well, there is one way to resist it - don't come here.

[Diane]

I have a part II to this idea. In the future I see the track being laid down now, as leading to clear concrete reasoning as to why manual therapy of any kind, from the lightest touch to the heaviest pressure, can help a nervous system downregulate pain. But for now, please bear with me as I lay down the paving stones.

This is a copy of a post I made to a discussion on another forum, slightly edited:
The question is,
"Why is it that if this analogy is true (that pain is a "need state" like that of thirst, requiring a "consummatory act", i.e., drinking =moving, or moving =drinking)....do we as humans have to rely on "techniques" to downregulate? Whereas thirst /need is essentially primal and reactionary....no need for such "guidance"?"

Earlier I supplied information re: "fishbrain" and secured your agreement that such an entity exists, both physically and "ph-unctionally". There were points made, summarized as follows:
1. Usually the non-conscious movement-producing parts of the brain get their own needs met automatically, by producing movement.

2. Non-conscious movement is the norm, not the exception. Sometimes, however, non-conscious movement production gets into trouble.

(These first two points are ones that Barrett takes great pains to include in his lectures, because his whole therapeutic intervention is based on restoration of non-conscious movement by deliberately inhibiting the inhibition of it.)

3. motor output is inherent in any living organism (i.e., embryonic), and is generated by it, before any sensory feedback can occur.

4. Later, in humans (who are living organisms it must be emphasized), sensory feedback and movement output blend together seamlessly to provide the ongoing illusion of control and self in a body. That's the normal non-painful state of affairs.

5. Pain is an output, generated by something that interferes with the combination of sensory input mixed with cognitive input mixed with body physiology/homeodynamics called the motivational affective input.

6. Pain INHIBITS movement we think we want to consciously make, because of mechanoreceptors having been sensitized.

7. The only way this system will produce the movement it needs to make is if the patient stops inhibiting their own corrective movement. Why do they inhibit it? Because they can. Because they don't know enough not to. Because it might look funny. Any number of reasons, usually unconscious.

8.NON-conscious is not the same as UN-conscious.
(Non-conscious is something a bit more physiological, autonomic, homeostatic or homeodynamic, whereas un-conscious has more to do with cognition and then forgetting why one ever thought something, or learned behavior that has gone on to become automatic.)

9. Pain is a signal that the non-conscious parts of the brain use to broadcast to the more conscious parts that it is perceiving a threat. See the thread called "Insula Matters" for more about how this occurs, via at least one structure that has good studies from less than a year ago.

Moving on, I think we can agree that the fishbrain is non-verbal. It does not understand language in any way, but it WILL react to handling, usually by trying to escape.

In order to understand why, I think it’s necessary to discuss the most fundamental sort of life-sustaining movement, breathing. The biggest threat to any brain, including the fishbrain from its own perspective, is hypoxia. (Does everyone concur? Does everyone agree that death of neural tissue occurs in only minutes without oxygen?)

The fishbrain is set up to signal itself about its own condition, more so than any other more evolved layer of brain, perhaps. Lets think about this for a moment:

Fishbrains evolved effortlessly extracting oxygen from seawater by swimming through it and letting the water flow through gills. Fish never had to catch, get, hold their breath or even breathe at all. But fishbrains did evolve the means for extracting oxygen and using it for metabolism. Movement equaled life, and stillness equaled death.

Through evolutionary time, more recent (but still non-verbal) land-living brain layers learned to deal with potential hypoxia by breathing (they INVENTED breathing), figuring out how to move against gravity, changing blood pressure, etc. Oxygen-exchange was still the biggest challenge they had to cope with, but nervous systems figured out how to deal with having to actively suck air in and wait for the next breath while exhaling the previous one.

I am saying that breathing is the most important job a nervous system (that has evolved beyond a fish brain) has, and fishbrains STILL know nothing of how go about breathing – all they can do is signal when they do not have sufficient oxygen. With me so far?

Slowly it is dawning on me that the reason most therapists seem to not understand this stuff is because maybe they can't easily see the human nervous system as a "collective", the collection of creatures we evolved through. Maybe not many are willing to suspend attachment to being "human" long enough to look at life from any other perspective, like, for example, from the perspective of a fish. I think to understand the nervous system experientially one must be willing to consider the matter from multiple viewpoints, from each "brain layer", each equally "alive", fighting to preserve its "life", and all deserving consideration.

[BB]

Diane,
Speaking of how for fish movement is required for life and breathing and how that relates to the non-conscious parts of our brain is an outstanding description.

I'm loving this info.

[Barrett Dorko]

I'm with Cory.

Perhaps one day I'll ask, "What happens when you try to catch a fish with your hands?" or "What exactly is the fascination so many have for fishing recreationally all about?"

[Diane]

Thanks. I think I'm finally able to understand the concept of "fishbrain" better myself...
Maybe one day I'll understand it well enough to be able to explain it to my grandmother. Meanwhile I think there actually might be a continuous story-line buried in here somewhere.
Move to liberate your inner fish. "Catch then let go" therapy

[Gil Haight]

Diane,
I'm having trouble trying to understand the part about how the fish brain level is trying to "get away". Once transcended is this behavior/characteristic acurately described as such?
Gil

[Diane]

Gil, what do you mean, "once transcended"? Do you mean, evolved away from?

[EricM]

I really like this definition of pain. It's so simple!

Pain is a signal that the non-conscious parts of the brain use to broadcast to the more conscious parts that it is perceiving a threat.

[Diane]

I see I am grammatically incorrect. It should read, Pain is a signal that the non-conscious parts of the brain use to broadcast to the more conscious parts that they are perceiving a threat.

[nari]

I like it too. Is much simpler than the IASP definition and sends a clearer message than the latter does.

Nari

[Diane]

Thank you Nari and Eric.

Here is some more information, some of it supplied by Cory, and some by me. (Slightly edited.)

First, Cory's contribution:
From Clinical Neurodynamics by Shacklock: This adds to what Diane is saying about the importance of oxygen to the nervous system and what this has to do with neurodynamics.

p17:
"Tension in nerves produces a reduction in intraneural blood flow. At 8% elongation, the flow of venous blood from nerves starts to diminish and at 15%, all circulation in and out of the nerve is obstructed"

Lundborg G, Rydevik B 1973 Effects of stretching the tibial nerve of the rabbit: a preliminary study of the intaneural cerculation and barrier function of the perineurium. Journal of Bane and Joint Surgery 55B: 390-401

Ogata K, Naito M 1986 Blood flow of peripheral nerve effects of dessection, stretching and compression. Journal Hand Surgery 11B(1): 10-14

"The blockage is caused by stretching and strangulation of the intraneural vessels."

Denny-Brown D, Dohery M 1945 Effects of transient stretching of peripheral nerve. Archives of Neurology and Psychiatry 54(1): 116-129

"Time is also an important factor in intraneural tension. If nerves are held at only 6% strain for one hour, nerve conduction reduces by 70%. If the duration of the stretch is increased, greater ischaemia and a longer recovery time will eventuate."

Effects of compression
"The failure threshold for compression is approximately 30-50 mmHg. In cases where pressure exceeds this value, hypoxia and imairment of nerve blood flow, conduction and axonal transport occur."

Gelberman R, Szabo R, Williamson R, Hargen S, Yaru N, Minteer-Convery M 1983 Tissue pressure threshold for peripheral nerve viability. Clinical Orthopeaedics and Rleated Research 187: 285-291

Rempel D, Dahlin L, Lundborg G 1999 Pathophysiology of nerve compression syndromes: response of periheral nerves to loading. Journal of Bone and Joint Surgery 81A(11): 1600-1610

"Compression of nerves is a normal part of human movement. Therefore, it is clear that normal movement does not usually produce sufficient compression to impair physiological functions. However, in a nerve with prior compromise, changes in pressure of a magnitude smaller than that in normal nerves could be sufficient to produce neuropathic symptoms with normal neurodynamic forces."

If the fishbrain does not "breathe" (and we know it doesn't because it has no lungs) instead it moves through water which passes over its gills - by some mechanism, probably similar to what happens in lungs, oxygen is "grabbed" by the blood flow of the fish across gill membranes and circulates around within the fishes body. Therefore it feels oppressed and suffocated when it can't move.

I think Chapter 7 (http://www.somasimple.com/forums/showthread.php?t=4041) of the book, Autonomic Innervation of the Skin, one of the Burnstock series, written by Peter Holzer, provides support for the idea that the fishbrain can feed itself oxygen. The chapter has to do with how afferent fibers also have efferent autonomic capacities.

Abstract: This article reviews the roles of fine afferent nerve fibres in the local regulation of cutaneous blood flow and vascular permeability. Pharmacologically characterized by their sensitivity to capsaicin, these afferents take part in the autonomic control of vascular function by releasing vasoactive transmitters from their peripheral fibres. Calcitonin gene-related peptide appears to be the principal transmitter of afferent nerve -induced dilatation of arterioles whilst substance P and neurokinin A appear to be the major mediators of increased venular permeability. These actions are mediated by specific peptide receptors on the vascular system and can be manipulated by specific peptide receptor antagonists. Afferent nerve-derived peptides regulate cutaneous microcirculation not only by an action on the vessels themselves but also by interaction with other microvascular control systems. Notably, substance P and calcitonin gene-related peptide are able to influence the activity of mast cells and immune cells, activities which may reinforce the inflammatory process and raise the excitability of the afferent nerve fibres.

Peptidergic afferent neurons are primarily nociceptive neurons whose overall function is to maintain homeostasis in the face of irritation or trauma to the tissue. This role is greatly aided by appropriate changes in the microcirculation at the very site of stimulation, changes which can be propagated away from the site of irritation via local axon reflexes between collaterals of afferent nerve fibres. Hyperaemia and increased vascular permeability facilitate the delivery of macromolecules and immunocompetent leucocytes to the tissue and thereby promote defence and repair of damage. Peptidergic afferent nerve fibres may, in addition, contribute to the healing of injured tissue. In contrast, the role of these afferents during chronic inflammation may be to induce hyperalgesia and to cause perpetuation of the inflammatory process.

I don't know about you, but what I get from this is that the "fishbrain" (especially the PNS portion thereof) feeds itself, and always has. Want permeability of the venules? Drip out some Substance P and neurokinin A. Want more permeability of the arterioles? Drip out CGRP. It's a reflexive system, which is my main point. It's like the fishbrain doesn't really have a brain. It's on autonomic pilot. :D

Movement keeps this all propelled along. Why would you need anything more than some pattern generators in your spinal cord to keep you moving? Especially when moving helps passively oxygenate your little fish body? And when your muscles all just tug on each other and set each other into wavelike contractions through mechanical reflex action, because they are all seamlessly woven into one another, why would you need a brain to learn to differentiate your movement very much? Baby fish can swim, oxygenate themselves and catch bits of food as perfectly as adults from the moment they hatch.

Even in us, it still works this way. The fishbrain mostly feeds itself (as per Chapter 7) and pattern generators in the spinal cord can keep us moving. The segmental muscles around the spine are like the ones fish have, i.e. segmented, attached to each other, operating reflexively, not much hard drive required, as soon as the sensory nerves are myelinated a human baby can start learning (through feedback and trajectory correction) to move its spine like a human instead of like a fish. In any case, movement assists oxygenation of tissue and blood return - I doubt anyone could argue with that.

Lack of movement? Well, there will be some backup probably, inside nerves. Nerves do not have a backup lymph system, so they might be prone to compression inside their tunnel. This might just set off nervi nervorum. But as we know, this isn't enough to trigger anything except a danger signal to the cord. The human brain has lots of fibres dangling down into the cord that, in effect, tell afferents to shush. It can turn a signal up too, if it wants to, but it usually doesn't.

So, with lots of practice of sitting around, there is neural adaptation from "higher" centres, that block out or dampen signals from the fishbrain, always complaining because it's been made to sit still for 4 hours straight, reflexive input into the cord. It's not comfortable, but it's only way of communicating, i.e., signaling discomfort, is not being listened to. It can put up with a lot, and the "higher" centers can dampen the signal for a long time, but... if there should happen to be some extra stress, some straw breaking some camel's back, some extra hard drive needed to deal with a shocking life event - the dampers will work less efficiently. More of this cord info will become less inhibited until.... maybe the insula takes over and decides, "There's a threat in sector 16!"

If "higher" centers have learned to sit still, and the "lower" ones need to move in order to not become hypoxic, something's got to give, and it won't be the fishbrain.

[Cheryl Conard Haight]

Diane,
Yes, I mean evolved, but I have trouble with the "away from". As we evolve each successive step trandscends but includes, negates but preserves the lower level. I take this to mean that the new level (here amphibians, I guess) is capable of operating on the lower level but must maintain some of its' function to survive. The point is that the fish brain is not separate. It is now integrated, but is it still a fish brain?
I think these points are important because of something you said subsequently- "It can turn a signal up too, if it wants to, but it usually doesn't." I don't think that is true. Immediately following injury the BStem strongly facilitates the dorsal horn (part of central sensitization) and since the descending inhibition of of the dorsal horn is tonic, any interruption of this tonic activity is essentially facilatory.
My point in all of this is that there are times when it is entirely appropriate to ignore and override the segmental "fish brain" activity and there are times when it is not. Sorting this out by developing improved interoception is essential to successful therapy.
Perhaps we are saying the same thing.
Gil,
I'm on my Cheryl's site.

[Diane]

Yes, Gil, I think we are saying the same thing. Thanks for the item re: brain stem interaction. And you're right about there being no real "away from". Thanks for pointing to that. Instead we must learn to understand and live with our inner fish.

And those of us who are therapists must learn to interact with it, encourage its efforts to escape without inflicting more sensory-discriminative input destined to become upregulated because of being too overwhelming for the rest of the brain(s).

I think the motor activity and the sensory activity are so completely reflexive and hooked together that any input at all activates movement by the fish brain. This is evidenced by the hyperreflexia seen in the absence of inhibitory control, i.e., SCI, or in neurological conditions such as multiple sclerosis, where descending control is eroded.

When we have a "normal" nervous system, it's harder to imagine that this fishbrain exists with all its reflexive behavior, but it is so completely inhibited movement -wise, that often the only way it can signal is by persisting with afferent "danger" signals - which themselves, if not attended to, regularly, through permission to move, will build up to the point of being read by the non-conscious brain as a threat, then broadcasted to our conscious awareness as a pain perception.

[Gil Haight]

Diane,
Very much so. I'm reminded of Juhan's statement in Jobs Body. In its' most fundemental state the CNS is a mechanism which allows for a motor response to a sensory stimulation. This holds true at the first synapse (dorsal horn) as well as in the primary afferent through its' retrograde release of SP, CGRP ( neurogenic inflammation). It doesn't even need a synapse. Everything is designed to respond.
Gil

[Diane]

This holds true at the first synapse (dorsal horn) as well as in the primary afferent through its' retrograde release of SP, CGRP ( neurogenic inflammation)
The only thing I'd quibble about is that I think release of SP and CGRP are considered "normal". I think when body movement that would ordinarily support circulation is lacking, this stuff isn't washed out, instead it backs up and bother the afferents back up their axons. Would you agree?

[Cheryl Conard Haight]

I don't know. I understand this efferent activity in the afferent branch to be associated with the introduction of proinflammatory mediators or possibly through activation of alpha adrenergic receptors upregulated as a consequence of nerve insult or whatever(migraine). I have never considered how movement influences this peripheral activiy. Good question. Perhaps movement characterised by both agonist/antagonist comes into play here.
Gil

[Diane]

Yes, but what I'm saying is, the nerves do this all the time anyway, and usually it doesn't create a problem. So I don't think we can blame the substances themselves, entirely, for being the "cause" of inflammation, rather they are incidental perhaps. Found at the scene of the crime, but circumstantial evidence, not the actual criminals.

I'm trying to consider the ineffable, i.e., movement and its presence or absence, as perhaps the key factor. I'm doing a thought experiment.

[Luke Rickards]

Not sure if it fits well, but I'm reminded of this paper.

[Diane]

Oooohh, this looks good. Got anymore like that Luke?

[Luke Rickards]

Heaps, but I'll have to go searching.

[christophb]

Thanks Luke, I've actually been looking for something like this. I read an abstract similar to this a while back (may have been same one) and have been thinking about it since.

I've been also thinking about an article Diane posted a bit back in the Movement and pain/Pain and movement (http://www.somasimple.com/forums/showthread.php?t=4453)thread re: pain and motor system plasticity.

acute pain induced by capsaicin can acutely affect plasticity of the motor cortex induced by a tongue task (tongue protrusion). Pain induced by capsaicin impairs the changes in motor systems as evidenced by a decreased response to transcranial magnetic stimulation applied over the motor cortex on motor evoked potentials (MEPS)

Sensory–motor integration at a reflex level such as a motor withdrawal reflex in response to noxious stimuli (nociceptive response) is well understood. Persistent pain generally inhibits movement, and subjects will protect the affected area to limit movement. This inhibition may ‘act as a sort of motor ‘decerebration’ so as to allow the spinal motor system to freely develop protective responses to noxious stimulation’

I'm assuming this to mean guarding at the reflexive level of the spinal cord (is this fish brain?). I wonder why this does not come back automatically but can see the value of trying to get the brain to be more aware of sensory motor maps through skin deep treatments and thoughtful movement so this cortical inhibition can resolve and therefore also the guarding at a reflexive level. Perhaps I'm taking too many liberties in my interpretation or misinterpreting though. Does this sound right?

[Diane]

I'm assuming this to mean guarding at the reflexive level of the spinal cord (is this fish brain?)
Chris, yes, I'd count spinal cord as fishbrain. Anything a fish has, and that we have in common with them.

I wonder why this does not come back automatically

Maybe it can, and does, when ideomotor movement is unveiled.

but can see the value of trying to get the brain to be more aware of sensory motor maps through skin deep treatments and thoughtful movement so this cortical inhibition can resolve and therefore also the guarding at a reflexive level. Perhaps I'm taking too many liberties in my interpretation or misinterpreting though. Does this sound right? Sounds right to me.

The biggest nugget I've gleaned during this thought exercise is finally getting around to sifting through the differentiation between fish brain (purely aquatic) and the next stage up. The big difference is in how aquatic creatures oxygenate versus how land creatures oxygenate. Amphibians are truly an intermediate type - they have lungs but also can breathe right through their thin skins. I "knew" these little factoids before, but I never put them into the center of the puzzle before. Instead, I tried to organize information around "pain".

The space at the center is always going to be oxygen exchange, and how various complexities of nervous systems organize themselves around this overwhelmingly overriding problem/challenge. Everything else is mostly ... I hate to use the term "window-dressing", but from a physiological point of view, other needs or urgencies are more episodic and delays to their gratification less important.

If oxygenation (by the nervous system, of itself) is instead put centrally, then pain itself can make more sense, at every level from fishbrain nociception on up. Rule the circulatory system in, as the nervous system's willing butler, because it is the inner ocean that the fishbrain invented, and which we still rely on, even though we don't use gills to access it. Or maybe we do, maybe gills just went inward and became ... more numerous capillary membranes.

[Diane]

Check out Ginger Campbell's podcast #23 (http://cdn.libsyn.com/brainsciencepodcast/23lev-brainscience-Blakeslee.mp3), her interview with Sandra Blakeslee, author of "The Body has a Mind of its Own". Very enlightening. Interesting discussion on horseback riding and combining human body maps with horses'. Horses have peripersonal maps too. A kinesthetic conversation of a slightly different sort.

[Diane]

Here is a book, called (apparently) Your Inner Fish (http://www.amazon.com/Your-Inner-Fish-Journey-3-5-Billion-Year/dp/0375424474) by Neil Shubin, not yet published. Here is a blues song called The Devonian Blues (http://www.trollart.com/sound/devonianblues/index.html).

I just heard about these. I'm liking the lines of thinking I've unwittingly become part of lately. :)

[EricM]

A little more about Your Inner Fish (http://www.randomhouse.com/pantheon/catalog/display.pperl?isbn=9780375424472)

[Diane]

Thanks Eric - can't wait until that book becomes available. :)

I've been thinking about this whole sympathetic influence on cutaneous afferents lately. In Sympathetic Modulation of Cutaneous Sensory Receptors, Chapter 8 (http://www.somasimple.com/forums/showthread.php?t=4093) of Autonomic Innervation of the Skin, studies were done that raised or lowered sensitivity by raising or lowering sympathetic output.
Several studies have been done in humans to test whether cutaneous sensibility is modulated by sympathetic efferent activity. The most direct and easily interpreted of these studies was done by Kissin et al (1987), who tested tactile detection thresholds in subjects before and during stellate ganglion block or lumbar epidural sympathetic block. Each of the 10 subjects was being treated for persistent pain, but one had spontaneous pain or mechanical allodynia in the area used for testing tactile sensibility. Seven of the 10 subjects reported little or no reduction in their ongoing pain during the sympathetic block, so the reported changes in tactile sensibility appeared not to result simply from a reduction in a competing sensation (pain).

Kissin et al (1987) reported that the 6 subjects who received unilateral stellate blocks showed a mean decrease in tactile threshold of 49±9% on the blocked side and an increase in threshold of 10±8% on the non-blocked side. Four subjects who received a bilateral epidural block experienced a mean reduction of 46±11% on the painful side and 48±13% on the non-painful side. The observed changes in tactile threshold were not consistent with temperature changes resulting from the blocks.

The results from the subjects receiving unilateral blocks in this well controlled study suggest that the sensitivity of cutaneous mechanoreceptors is normally attenuated by ongoing sympathetic efferent activity in such subjects. The marked difference in the changes in tactile sensitivity on the two sides during stellate block suggests that nonspecific central effects were not responsible for the block-induced changes in threshold.

Is this increase in tactile sensitivity during sympathetic block explicable on the basis of findings from studies of sympathetic actions on cutaneous afferents? It is if one considers that Kissin et al tested tactile thresholds by brief application of von Frey filaments. Such stimuli are likely to activate both rapidly and slowly adapting mechanoreceptors such as hair afferents, Pacinian afferents, and SA I receptors. Their finding of decreased tactile thresholds during sympathetic block could be explained by a reduction in the mechanical threshold in any of these mechanoreceptors during interruption of ongoing sympathetic activity, or conversely, by increased thresholds during increased sympathetic activity. In fact, increased mechanical thresholds were found in both 'hair' afferents and subcutaneous Pacinian afferents during sympathetic stimulation in cats (Freeman and Rowe 1981; Pierce and Roberts 1981; Roberts and Levitt 1982).

So, what I get from this is that increased sensitivity in skin (i.e., painful places, mechanosensitivity in skin) is connected to an abnormally low amount of sympathetic function in the fish brain. Because only sympathetic efferents are found in skin (no parasympathetics), and because touching skin immediately raises sympathetic activity, there will be a corresponding rise in thresholds for sensitivity in "normal" systems (i.e., as long as they have no "channelopathies").

So, I'm thinking most benign pain, with its attendant mechanosensitization and abnormally low sympathetic efferent output, is essentially a symptom of "touch" deficiency.

Touch, contact, handling will immediately stimulate sympathetic effectors. That's nature. The systems (fishbrain and all the newer CNS layers) will ask, What is this? Is this a threat? Should I worry? One by one they will wink out upon deciding there is no threat. The fishbrain however, will continue to react, because it deals with local phenomena. Once the rest of the CNS let's go of it, and let's it get on with its job, it will. The peripheral sympathetics to the zone being handled will react. They'll be firing in two directions, centrally and peripherally.

Centrally, the brain will be curious but not threatened. It will probably start to feel relieved right away.
Peripherally, the sympathetics will do their best to counteract with everything they've got, but because it's so small an area of the two square meters of skin they have to deal with, what will happen is a containment exercise. The threshold of the cutaneous receptors will go up (just what we want), and the human bits of CNS (watching) will get even more interested in playing along, because they like being able to downregulate - it's what they like to do most. Keep that crazy fishbrain with no brain from spamming them with useless nociceptive info.

Getting the body to hurt less means getting the sympathetics back online. (Get the beer and the remote pried out of their lazy hands and flip them out of their hammocks, give them some jobs to do, get them active again.)

The easiest way to do this in a mechanosensitized person is through the skin, because 50% of the motor output from the cord is sympathetic, and most of that output is about skin and homeostatic, homeodynamic oxygenation/temperature regulation. The easiest way is by handling skin. Carefully, so the newer levels of CNS come over to your side, and precisely, to stimulate the fishbrain in dosed amounts, to give that sympathetic portion of it graded exposure to rousing itself, give it a workout, allow it to accomplish downregulation of cutaneous afferents. Gently, so it is not overwhelmed. Rehabbing it. Here. Then here. Then over here. Once downregulated by the local sympathetics, cutaneous afferents will tolerate rougher handling, but not before.

So, why stimulate the sympathetic nervous portion of the fishbrain? To get it to do its job. What is its job? to prepare skin for battle. How? By desensitizing it (down regulating nociceptive sensitivity) so the brain can focus on more important things. By changing blood flow within it, i.e. decreasing it to limit blood loss. By in-creasing blood flow to muscle and by extension other mesodermal subcutis structures, including neural tunnels. Why? So that the nerves have increased perfusion/oxygenation to help out, so that muscles can pump up to help the organism get away or fight.

When palpating skin you can feel all this battle preparation occurring. It feels quite dramatic sometimes. The main objective is to get something, anything to happen, palpably. When it does, you can surmise that the system is self-correcting, that it is downregulating, that it is self-regulating its chemistry, receptors, channels, all those peptides and everything that has gone wrong for long periods of time, making patients feel awful from pain but not quite able to get themselves better. The CNS can't quite get through to to the fishbrain sometimes to downregulate it successfully.

Sometimes, a carefully dosed and contained and managed and provided "external threat" is required before the fishbrain will respond with all its sympathetic arousal potential, so that it can self-correct. It responds most readily and successfully to kinesthetic input, to kinesthetic conversation - as its therapist you definitely want it to talk back, try to kick you out, express itself fully, take its tasks back up, get back on track, find its purpose in life again, become functional, feel successful, be restored to its place in that larger entity that it was kept as part of because of the importance of its task. In fact, one could see physical therapy as relationship counseling for all the various aspects of a nervous system that have come to find themselves at odds with each other. Human primate social grooming of a most basic sort. Being a translatory bridge to help systems integrate into a happier neuromodular family.

[Diane]

Does anyone remember the song, Dangling Conversation (http://youtube.com/watch?v=IdodDEELLDg) by Simon and Garfunkel? To me it speaks of richness of life juxtaposed against boring meaninglessness - sort of like how the PT profession is poised perfectly to be able to take on board really good pain-relieving manual treatment, but doesn't because of the "borders of our lives". So most patients are left to deal with dangling kinesthetic conversations.

Plus, much of PT becomes dangling kinesthetic conversation conducted at this sort of speed (http://youtube.com/watch?v=CgnWMwt-ewc). :sad::thumbs_do

I propose that good manual contact resolves inner dangling conversations between and among brain parts, and collectively between brain parts and the more peripheral fishbrain part.

[Luke Rickards]

So, what I get from this is that increased sensitivity in skin (i.e., painful places, mechanosensitivity in skin) is connected to an abnormally low amount of sympathetic functionDiane,

Do they go on to state that hyperalgesia/allodynia is a result of a hyposympathetic state?

The way I read the sensitivity of cutaneous mechanoreceptors is normally attenuated by ongoing sympathetic efferent activity in such subjects. is that persistent pain subjects with sympathetic hyperactivity have lowered cutaneous sensitivity as a result. This can be improved (I didn't see anything about it becoming sensitive above normal) by reducing the sympathetic efferent activity.

Looking forward to more....

[Diane]

About this question, (speaking of dangling conversations):
"Why is it that if this analogy is true (that pain is a "need state" like that of thirst, requiring a "consummatory act", i.e., drinking =moving, or moving =drinking)....do we as humans have to rely on "techniques" to downregulate? Whereas thirst /need is essentially primal and reactionary....no need for such "guidance"?"

Good question.

Do fish/fishbrains get thirsty? The answer is, they drink all the time and have saline filtering strategies, so they don't get thirsty. But other brain parts (that evolved later) do create thirst. Why? because they came along after transition to land, where conditions dictated that only brains that could successfully downregulate need states would survive. This means, waiting until you can get to the waterhole before you can have a drink. This means, waiting until the lions have eaten someone else before you can safely drink with your back turned. This means, waiting for the crocs to move away from the bank you are on, toward more vulnerable (thirstier) pickings.

I feel another contemplative episode coming over me. Thirst is next on the hierarchy of need states, right after oxygenation. Think about how you can't go without oxygen for more than a few minutes. Think about how you can't go without fluid replacement for more than a few days.

Fish do not need to replace their fluids through any action program (as per Melzack's neuromatrix diagram) because for them, fluid replacement is a completely automatic process. All they have to do is swim. But - fishbrains that have taken up residence in the inner sea of human beings and other land creatures DO have fluid issues. They must deal with fluctuating fluid levels, in fact. A lowered fluid level will impact their normal function. If fluid volumes drop blood will thicken and not get around as easily. Evolution took care of this by installing some signals to warn the "advanced version" nervous systems of impending danger, i.e., through creating the warning signal of thirst. Increasing thirst signals will come up the need hierarchy until the need to drink becomes overwhelming, croc or no croc.

So the thirst/pain analogy is a contrivance, an analogy, a comparison, useful only to a point. There is no real correspondence there, just a metaphor so that people can "get" the meaning of pain state being a need state or a "danger" state or a physiological "threat recognition" state of sorts.

At the level of the fishbrain, the metaphor fails, which makes pain and a manual therapeutic approach, a kinesthetic conversation approach to it, hard to grasp. It's a lot easier if you look at what the fishbrain requires, and help it do what it needs to do. It doesn't really feel "thirst", but it feels nociception. In a sense it IS nociception. It is also the solution to nociception - it is the sympathetic peripheral nervous system, which when activated will self-correct ordinary mechanosensitization.

It needs to actively try to "escape" at many different loci. In fact, one could conceptualize visually the entire distributed human sympathetic PNS as a whole school of fish, not just one fishbrain. It's a collective. Selected individual fish (individual receptive fields) have to be prompted to enact escape behavior until finally the whole school decides to take off as a group, whereupon downregulation can become complete, but without any suppression of peripheral physiology, in fact, ordinary function restores itself once the "fish" are prompted into doing what they should be capable of, and behave accordingly i.e., self-correct.

[Diane]

Luke,

Quote:
So, what I get from this is that increased sensitivity in skin (i.e., painful places, mechanosensitivity in skin) is connected to an abnormally low amount of sympathetic function
Diane,

Do they go on to state that hyperalgesia/allodynia is a result of a hyposympathetic state?

The way I read
Quote:
the sensitivity of cutaneous mechanoreceptors is normally attenuated by ongoing sympathetic efferent activity in such subjects.
is that persistent pain subjects with sympathetic hyperactivity have lowered cutaneous sensitivity as a result. This can be improved (I didn't see anything about it becoming sensitive above normal) by reducing the sympathetic efferent activity.

Looking forward to more....

I finally figured out in this excerpt from Chapter 8 (took me long enough) that sensitivity is inversely proportional to threshold (a small eureka moment, then it passed). I think "in such subjects" refers to those tested with sympathetic blocks.

The way I read it is that when the sympathetics are blocked from working, sensitivity goes up, i.e., threshold goes down. When the block to sympathetics is NOT there, the threshold goes back up, and sensitivity goes down.

That's how it makes sense to me now. Also, I remember a long while ago, reading in Topical Issues in Pain, a piece by Mick Thacker that made absolutely no sense to me at the time, about how pain decreases with a rise in sympathetic action. Now it makes much more sense. At least at the moment it does.

[Luke Rickards]

Yes, I am aware of the relationship between sensitivity and receptor threshold.

I'm still wondering though, is there more on the conclusion that hyperalgesia/allodynia is a result of a hyposympathetic state, as stated in "increased sensitivity in skin (i.e., painful places, mechanosensitivity in skin) is connected to an abnormally low amount of sympathetic function"?

[Diane]

I suppose there must be. I will try to dig them up.

I think it would be good to examine the assumption that "sympathetically maintained pain" is due to too much sympathetic activity, when in fact, this stuff seems to suggest that "sympathetically maintained pain" might be due to sympathetic deficiency instead. Then deconstruct it if that's what is needed.

We need to find Kissin et al 1987; Freeman and Rowe 1981; Pierce and Roberts 1981; Roberts and Levitt 1982
I will find out the names of the articles we need.

[Luke Rickards]

I wonder why all surgical and pharmacological interventions directed at the SNS in pain patients attempts to decrease sympathetic tone. Surely if sympathetic stimulation was the key, someone would have tried it by now? (I looked, but maybe not hard enough)

[Diane]

I think those interventions came about pre-Wall/Melzack deconstruction. And I think there is a pretty high failure rate with them too. :)

[Luke Rickards]

That is true. But still, no one is stimulating the sympathetic ganglions instead.

[Diane]

Luke, no one is stimulating the sympathetic ganglions instead. How? Why would anyone need to? We can stimulate those mechanosensitized lowered threshold exteroceptors instead, without adding more gas to the fire, and get the fire to put itself out instead. Out in the skin. Let the ganglia look after themselves...
They are potentially "normal" aren't they?

[Luke Rickards]

I wasn't referring to us. I was referring to the people who do the type of research we are talking about. The people with the machines and needles and drugs at their disposal.

[Diane]

Ok. I thought for a minute you were talking from a generic mobilipulator persepective of the chiro sort - those who think they can stimulate a single select ganglion of either the sympathetic persuasion or the dorsal root persuasion. Now I see what you mean. :)

I think bringing more info will definitely help the hyper or hypo sympathetic issue we have uncovered to resolve.

[Luke Rickards]

I'm on to it too. Though it's nearly bed time here.

(Don't know why you would think I was coming from that perspective :p )

[Diane]

We need:

1. Kissin I, McDanal J, Brown P T, Xavier A V, Bradley EI (1987). Sympathetic blockade increases tactile sensitivity. Anesthesia Analgesia 66, 1251-1255

2. Freeman B and Rowe M. (1981). The effect of sympathetic nerve stimulation on responses of cutaneous Pacinian corpuscles in the cat. Neuroscience Letters, 22, 145-150.

3. Pierce JP and Roberts WJ (1981). Sympathetically induced changes inthe responses of guard hair and type II receptors in the cat. J.of Physiology (London) 314, 411-428.

4. Roberts WJ and Levitt GR (1982). Histochemical evidence for sympathetic innervation of hair receptor afferents in cat skin. J. of Comparative Neurology 210, 204-209.

[Diane]

Don't know why you would think I was coming from that perspective
I know, you're not one 'o them. Please forgive my insula for registering an irrelevant threat signal. :)

[Luke Rickards]

These are quite old and we may not have access to the fulltext. Have a look though.

[Diane]

Yes. They may require an actual trip to some library and some real-time photocopying. :)

Here is a link to a very old thread (http://www.somasimple.com/forums/showthread.php?t=1308&highlight=Mick+Thacker) on the topic of sympathetically maintained pain, the very chapter I was thinking about earlier.

[Diane]

Just so we are clear, when I refer to "fishbrain" I'm including only the somatic peripheral nervous system and the spinal cord reflexive centers that automatically regulate it. See more about that here (http://www.somasimple.com/forums/showthread.php?p=40637#post40637).

[Diane]

Here is a link (http://www.somasimple.com/forums/showthread.php?p=40742#post40742) to the Kissin article listed in Post * 42 (http://www.somasimple.com/forums/showpost.php?p=40605&postcount=42).

Here is a link (http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=7310696) to article #3 also listed in # 42.

The other two articles are physical go fetch ones.

I have to ponder these with Luke's help for awhile before I can post anything intelligent about them. If anyone else would like to try, please feel free. :)

[Luke Rickards]

Here is the key from Kissin (http://www.somasimple.com/forums/showthread.php?t=4520) -

The decrease of touch threshold induced by sym-
pathetic block in normal skin demonstrated in our
study and the therapeutic effect of this type of block
in allodynia and hyperpathia (1,2) may be regarded
as contradictory results. However, they do not seem
to be conflicting within the framework of the follow-
ing hypothesis. Sympathetic efferent action on cuta-
neous mechanoreceptors, specialized to detect touch,
transforms them into less specific receptors, provid-
ing both tactile and painful sensations. These mod-
ulated receptors are less specific for touch, and there-
fore tactile sensitivity mediated by them is decreased.
On the other hand, being low-threshold mechano-
receptors, they provide painful sensation to stimuli
that have energy intensity greatly below the tissue-
damaging level. How can sympathetic efferent action
convert mechanoreceptors specialized to detect touch
into receptors signaling pain? It is possible to suggest
that the sympathetic nervous system can do it by
modulating the process of coding of tactile stimuli in
the mechanoreceptors. The coding theory of pain sen-
sation opposes the view that pain is a “specific mo-
dality” with specialized sensory end organs (21,22).
Presently, evidence for the concept that mammalian
cutaneous receptors are specialized for nociception is
prevailing (23). However, in any case it is conceivable
that strong sympathetic modulation may switch no-
ciception into a phylogenetically older, less special-
ized way of functioning when the same receptor is
responsible for both touch and pain.

[Diane]

Luke, are the slowadapting TypeII mechanoreceptors in skin part of this?
Also I wonder (still have to digest the article) what exactly is being blockaded: Is it efferents from the ganglia out to periphery/skin, or descending fibres to the ganglia within the cord, or both at once?

[Luke Rickards]

are the slowadapting TypeII mechanoreceptors in skin part of this?I don't know, Diane. They didn't mention it.

what exactly is being blockadedThe sympathetic ganglia (the stellate in this case) are where the synapses are located. A block inhibits transmission across the synaptic junctions.

[Gil Haight]

HI all,
I have always found this sympathetic thing to seem convoluted. Consider this. CRPS ( sympathetic reflex, SMP) is often treated with Clonidine, a alpha receptor agonist! How about the fact that peripheral sensitization involves vasodilitation and sympathetics vasoconstrict.
Lukes question about whether sympathetic activity(reduced) by itself can cause allodynia is the central question.
I think Kissin's comments have something to do with Craigs concept of homeostatic emotions. I dont' have time to comment now, but hope to later.
Very interesting thread, Diane.
Gil

[Luke Rickards]

I used to think that when the SNS was ramped-up, all SNS neurons were being activated. The info here and elsewhere over the last few months has indicated that this isn't the case at all. Some situations require a reduction of certain SNS neurons and, at the same time, a stimulation of others, eg hot weather involves stimulation of sudomotor neurons and inhibition of vasoconstrictor neurons.

I have no doubt the SNS's role in pain is no less complex.

[Gil Haight]

Luke,
Excellent point. Pts. who respond well to Simple Contact become warm (reduced sympathetic) and diaphoretic (increased sympathetics). I recognise that there different receptors involved here but still.

Back to Craigs homeostatic emotion concept. According to his theory, pain is not a sensation, a subset of touch, because of how it is processed centrally. Experiences such as pain, thrist, hunger, temp regulation and sexual pleasure like position sense or light touch (low threshold mechanoreceptors) involve a relay in the thalamus. However the former also involve the insula whereas the latter are sent to the sensory-motor association cortex. They, pain and touch are quite literally different phenomenon. Is it possible that the ANS has something to do with this processing from the very beginning?
Gil

[Diane]

Gil, I'm glad it's not just me who finds this whole autonomic thing convoluted, if not terminally confusing. Is it possible that the ANS has something to do with this processing from the very beginning? Good question. Peripheral ANS I take it you mean? It must I think, because evolutionarily it preceded most of the CNS and likely most if not all of the cortex/descending modulators. In the beginning there was the nerve net, and later fish built vertebral columns to house processors.

[Gil Haight]

I guess one way to look at all of this is to recognise that as levels are added the basic structure of afferent/efferent fusion is maintained. Deeper and more complex, yet fundementally consistant.
Diane, your metaphors are truely remarkable.
Gil

[Diane]

Remarkable good or remarkable bad...? :rolleyes:

Anyway, when I'm confused or when something seems paradoxical, I always comfort myself by returning to basic facts, like from Gray's.

The entire nervous system and the special sense organs originate from three sources each derived in turn from specific regions of the early epiblast generally termed neural ectoderm. The first source to be delineated is the neural plate which forms the CNS, the somatic motor nerves, and the preganglionic autonomic nerves.

The second source is from cells at the perimeter of the neural plate which remove themselves by epithelial/mesenchymal transition from the plate just prior to its fusion into a neural tube; these are the neural crest cells which form nearly all of the PNS, including the somatic sensory nerves, the somatic and autonomic ganglia, postganglionic autonomic nerves, and adrenal and chromaffin cells; they also give rise to significant mesenchymal populations in the head.

The third source is from ectodermal placodes; these are groups of cells which originate at the edge of the neural plate but remain in the surface ectoderm after neural tube formation undergoing epithelial/mesenchymal transition after the neural crest cells have commenced their migration. Ectodermal placodes contribute to the somatic sensory ganglia of the cranial nerves, to the hypophysis. the inner ear and, by a non-neuronal contribution, to the lens of the eye.

Anything that comes from neural crest is going to be more neurochemical, more paradoxical. It seems like it just has more scope, more capacity for being adaptable to the needs of the moment. More shape-shifty. By contrast neural plate and ectodermal placode derivatives are more fixed from the start to be electrically signally, more defined, less adaptable except by pruning via glia which themselves come from neural crest. Neural crest is just plain weird and malleable like clay. It seems to me to be the most "plastic" stuff in all of the nervous system. It can disguise itself as mesoderm if it wants, but still retains connection to the nervous system, signals it. And cells that are from neural crest sprinkle themselves all over the place, and comprise the entire PNS. It really does seem like it's its own creature in many ways, with its own behaviour. Neural crest is most of the fish brain.

I still don't know what's going on in sympathetic blocks. I guess my next question would be, are the preganglionic neurons prevented from talking to the postganglionic neurons? Is that what is happening with a blocking technique in a sympathetic ganglion? I wonder how good the communication is in there in the first place in pain states. It's like a whole other series of "chat rooms" alongside DRGs.

[Jon Newman]

This paper (http://www.pnas.org/cgi/content/abstract/103/7/2416) addresses the thirst/pain issue a bit. You should be able to get the full text free.

[Diane]

Here is a lengthy article on the evolution of the amygdala (http://www.blackwell-synergy.com/doi/full/10.1111/j.1469-7580.2007.00780.x). The amygdala is part of the basal ganglia, next step up from. It is not a monolithic structure, has at least 4 histologically distinct components, living in close proximity. It suggests a number of interesting avenues for thought and for further investigation, but concludes that fish (and likely our fish ancestors) do/did not possess actual amygdalas/amygdalae (go to the section called "Is there an amygdaloid complex in fish?"). The function of the amygdala is to take raw sensory info and be the first line of descending info to alert the body to prepare autonomically for fight or flight (sympathetics). (See Ramachandran's latest video (http://www.ted.com/talks/view/id/184) for a discussion of Capgras syndrome, or what happens when the "wire" from raw visual centers to the amygdala is cut.)

But what if fish don't have much in the way of raw sensory data to process? Their watery environment provided them with everything they needed, including continuous oxygen, continuous taste, and continuous bouyancy, very little contrast via vision. They developed sharp escape behaviours, because the biggest contrasting sensory input they would have had would have been through their integument.

Hodological data in teleosts indicate that a region of the subpallium receives primary and secondary olfactory fibres (Matz, 1995; Folgueira et al. 2004) and projects to other subpallial regions, the hypothalamus and the posterior tubercle (Shiga et al. 1985; Folgueira et al. 2004), resembling the case of the MeA in anurans (Moreno & González, 2003). This evidence does not support a clear homology with the vomeronasal amygdala of tetrapods but at least suggest the existence of an ‘early amygdaloid area’ in the subpallium of fish (at least as a field homology) (Folgueira et al. 2004). Therefore, the acquisition of a real vomeronasal amygdala would have taken place in the ancestral amphibians.

To me, this makes sense in that fish rely more on "taste" (of their surrounding water habitat) than on smell. Smell didn't need to differentiate until life on land became a necessity, and picking up odors wafted through a much less dense medium, i.e., air, became a necessity/evolutionary selection pressure. Still, fish had a few teeny brain bits that eventually gave rise to that which would eventually become amygdala.

I think this info relates to this thread, because of how we are trying to help a human primate brain gain control over sympathetics, among other things, that have gone awry in the fish brain (the sensory motor and autonomic ganglia and spinal cord, primitive to the "body")*, while simultaneously dealing with all the complex and maximized body maps that exist upstairs as they review and revise their sequencing, no doubt revisiting how to downregulate each other optimally. I'm going over this info with a fine toothed comb, in the never ending quest to become a better "informed desensitizer (http://www.somasimple.com/forums/showthread.php?t=114&highlight=Zusman)", in the words of Max Zusman. Much of the time I feel as though on the outside of someone's body, I'm merely holding up a flashlight so the brain can fix its own motor. A humble task, but helpful from the brain's perspective, as it is the sensitized mechanoreceptors (in ordinary persistent pain problems) that need the most work done. (See Chapter 58 (http://www.somasimple.com/forums/showthread.php?t=4248), post #2 (http://www.somasimple.com/forums/showpost.php?p=37764&postcount=2).)

* “…part of the brain is common to and essentially unchanged throughout all vertebrates, and is responsible for all of the sensory–motor reflexes and purely instinctive behaviors necessary for survival. This is the palaeëncephalon, which constitutes the entire fish brain. During the course of subsequent evolution, a new layer is added, the neëncephalon, which corresponds to the cerebral pallium. This is tiny in amphibians, a little bigger in reptiles, considerably larger in birds and huge in mammals. According to this model, brain evolution took place in a geological fashion by the addition of strata.” - Larry Swanson, "What is the Brain?"

[Diane]

Jon, I found the paper you mentioned above in post 57, and a whole bunch of others as well, which I'll examine and bring. It all came back round to the insula, which figures.

Meanwhile I found a new blog, well new to me anyway, called Frontal Cortex (http://scienceblogs.com/cortex/) by Jonah Lehrer (http://www.jonahlehrer.com/About%20Me%202.html) (who looks to be somewhere between 14 and 15 years of age....), wherein I searched "pain, insula" and it gave me 25 titles (http://scienceblogs.com/cortex/fastsearch?order=date&IncludeBlogs=42&search=pain%2C+insula). In the list I found a post called Sin Dolor (http://scienceblogs.com/cortex/2007/10/sin_dolor.php), wherein I found a link to this article on a specific channelopathy (http://www.somasimple.com/forums/showthread.php?p=41204#post41204) that prevents a person from feeling pain.

I immediately wondered if there would ever be any way to test to find out if what we do helps a brain of a patient in pain plug up this channel in some way.

[BB]

Maybe this is obvious to everyone, but "sin dolor" is spanish for "without pain."

[Diane]

I think I'm getting closer. Here a really good paper from 2003, by Pietro Cortelli (http://kubicov.lib.bioinfo.pl/auth:Cortelli,P), called Chronic pain and autonomic interactions (http://www.somasimple.com/forums/showthread.php?p=41227#post41227).

[Diane]

This paper (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15182741&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum) answers a question for me. It explains why it takes a bit of time between the introduction of a small amount of lateral stretch and decrease of perceived pain, and how the autonomics may be involved. Göteborg, Sweden is where Jänig is located as I recall.

1: Auton Neurosci. 2004 Apr 30;111(2):116-26.
Does sympathetic nerve discharge affect the firing of myelinated cutaneous afferents in humans?
Elam M, Macefield VG.

Institute of Clinical Neuroscience, Sahlgren University Hospital, S-413 45 Göteborg, Sweden. mikael.elam@neuro.gu.se

In clinical practise, the notion that some complex regional pain syndromes (CRPS) are associated with sympathetic facilitation of nociceptive transmission is widespread. However, physiological increases in cutaneous sympathetic nerve activity have not been found to influence the firing properties of cutaneous polymodal nociceptive (high-threshold mechano-heat sensitive) fibers in human subjects. Whether the same applies to low-threshold cutaneous mechanoreceptors is not known. Such an effect could be relevant for sympathetic facilitation of nociception, given that tactile afferents are implicated in the allodynia associated with CRPS. This issue was addressed by recording the responses of single cutaneous mechanoreceptors in the glabrous skin of the finger pads to constant mechanical stimuli, at rest and during physiological increases in cutaneous sympathetic activity produced by arousal stimuli. Unitary recordings were made from 17 rapidly adapting (15 FAI and 2 FAII) and 20 slowly adapting (9 SAI and 11 SAII) afferents located in the finger pads via tungsten microelectrodes inserted percutaneously into the median nerve at the wrist in nine subjects. A servomotor applied 1 s constant-displacement ramp-and-hold indentations to the receptor-bearing digit every 3 s. Displacement and compression force were recorded. Blood flow in the finger pad and sweating in the palm were measured contralaterally. Increases in cutaneous sympathetic outflow caused only modest changes in the spontaneous and compression-evoked firing of tactile afferents. These changes were usually (for 26/37 afferents) related to the associated decreases in skin blood flow. The latency from the start of the ramp stimulus to the onset of firing was inversely correlated to flow (i.e. unit response was delayed during vasoconstriction) for 11/31 units (7/15 FAI, 1/2 FAII, 2/9 SAI, 1/5 SAII), whereas no units showed a positive correlation. Compression-evoked firing rates were positively correlated to flow (i.e. vasoconstriction reduced firing rates) for 14/31 units (2/15 FAI, 1/2 FAII, 7/9 SAI, 4/5 SAII), whereas no units showed a negative correlation. 10/11 SAII afferents exhibited spontaneous background firing, which increased for 4 and decreased for 4 in response to arousal stimuli, presumably reflecting their sensitivity to changes in skin stretch associated with sympathetically mediated reductions in blood volume in the finger pad. Two afferents showed no change, but nor was there significant vasoconstriction in these recordings. Thus, arousal stimuli reduced rather than augmented tactile afferent firing. The close relation to blood flow for all types of afferents, and the different responses among SAII afferents, suggest that sympathetically mediated changes in afferent firing properties are indirect, i.e. secondary to changes in the mechanoreceptors' tissue environment rather than to a direct sympathetic effect on the endings.

Thank you for this, Elam and Macefield. :)

[BB]

Nice find, Diane! Help me make sure I've got what they are saying.

-sympathetic arousal from mechanical stimulation

-caused vasoconstriction

-thus decreased local blood flow

-which decreased afferent activity

Did I get it?

[Diane]

Well, I don't think it's entirely conclusive, but I'm so glad to see someone trying to work out the connections between afferents, blood flow, stimulation by skin stretch. Sympathetics do it all (they are all there is in the periphery) - they have to do both vasoconstriction and dilatation.

I think you got out of it what I got out of it. I don't think they can entirely blame tactile afferents for CRPS, because there's rumored to be a big inverse neuroplasticity factor in S1 happening in that condition (Moseley). However, something happens and blood flow starts to move, mechanoreceptor environment changes. Tactile afferents sensitivity became reduced. Which has to be good. I think.

[Diane]

Luke, what do you think?

[Luke Rickards]

I have just uploaded the full file here (http://www.somasimple.com/forums/showthread.php?p=41409#post41409) . I didn't feel like I could properly comment on this paper from the abstract alone.

Important stuff we didn't get from the abstract-
These were healthy subjects.
The sympathetic stimulus was not mechanical, but a cold spray in the face or mental arithmetic.
The conclusion is that sympathetic stimulation actually counteracts the effects of neurogenic inflammation.

I recommend reading section 4.2 and 3. Very interesting.

The important stuff for Diane is -The majority of human SAII endings respond to planar skin stretch with an increased firing in one axis of stretch and a decrease in the orthogonal axis (Johansson and Vallbo, 1983). In a study of SAII afferents in the hairy skin of the cat, (Pierce and Roberts, 1981) found that only those SAII endings sensitive to stretch perpendicular to the long axis of the leg increased their discharge during electrical stimulation of the sympathetic chain. Moreover, these receptors increased their background discharge without increasing their sensitivity to mechanical stimuli (Pierce and Roberts, 1981). These changes could be explained by changes in vascular filling [which] would affect the leg circumference. Unfortunately, we do not have data on the preferred directions of planar skin stretch to which each of the SAII afferents recorded in the present study responded, so we cannot correlate the sign of the change in mean firing rate with the orientation of the receptor within the skin. However, for the two SAII endings that did not change their firing after the sympathetic stimulus, it is worth pointing out that there were no associated vasomotor responses (although sudomotor responses were present).Looks like we need to get Johansson and Vallbo, 1983.

[Diane]

Thank you so much Luke. I will go and compost this excellent info, and come back to it once it all/if it all starts to make sense to me. :angel:
I think the implications are big.

[Diane]

I see that the title alone puts me into a bit of cognitive dissonance.
The title is, "Does sympathetic nerve discharge affect the firing of myelinated cutaneous afferents in humans?"

I realize I am trying to translate that into "Does the firing of myelinated cutaneous afferents in humans affect sympathetic nerve discharge?"

[Diane]

"Mechanosensation" (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16079835&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum). Knowing the name of something sure helps in finding material related to it. ;)

Nature. 2005 Aug 4;436(7051):647-54.
A possible unifying principle for mechanosensation.
Kung C.

Laboratory of Molecular Biology and Department of Genetics, University of Wisconsin, 1525 Linden Drive, Madison, Wisconsin 53706, USA.

Of Aristotle's five senses, we know that sight, smell and much of taste are initiated by ligands binding to G-protein-coupled receptors; however, the mechanical sensations of touch and hearing remain without a clear understanding of their molecular basis. Recently, the relevant force-transducing molecules--the mechanosensitive ion channels--have been identified. Such channel proteins purified from bacteria sense forces from the lipid bilayer in the absence of other proteins. Recent evidence has shown that lipids are also intimately involved in opening and closing the mechanosensitive channels of fungal, plant and animal species.

[Diane]

This looks like a promising article (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15362151&ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum) for this thread:
1: J Neurobiol. 2004 Oct;61(1):30-44.

Mechanosensation and pain.
Lewin GR, Moshourab R.

Growth Factors and Regeneration Group, Max-Delbrück Center for Molecular Medicine, Robert-Rössle-Str. 10, Berlin-Buch D-13092, Germany. glewin@mdc-berlin.de

The ability of cells to detect and transduce mechanical stimuli impinging on them is a fundamental process that underlies normal cell growth, hearing, balance, touch, and pain. Surprisingly, little research has focused on mechanotransduction as it relates to the sensations of somatic touch and pain. In this article we will review data on the wealth of different mechanosensitive sensory neurons that innervate our main somatic sense organ the skin. The role of different types of mechanosensitive sensory neurons in pain under physiological and pathophysiological conditions (allodynia and hyperalgesia) will also be reviewed. Finally, recent work on the cellular and molecular mechanisms by which mechanoreceptive sensory neurons signal both innocuous and noxious sensation is evaluated in the context of pain.

[Diane]

Here is some more info on mechanosensation and pain. It's all open access.

Mostly it's about channels and genes etc, but I'm going to go look for articles to do with skin stretch and mechanosensation.

[Diane]

Only one bite: here is it: Physiol Behav. 2007 Sep 10;92(1-2):21-8. Epub 2007 May 25.
Mechanotransduction and the crayfish stretch receptor.
Rydqvist B, Lin JH, Sand P, Swerup C.

Karolinska Institutet, Department of Physiology and Pharmacology, S-177 71 Stockholm, Sweden. bo.rydqvist@ki.se

Mechanotransduction or mechanosensitivity is found in almost every cell in all organisms from bacteria to vertebrates. Mechanosensitivity covers a wide spectrum of functions from osmosensing, cell attachment, classical sensory mechanisms like tactile senses in the skin, detection of sound in hair cells of the hearing apparatus, proprioceptive functions like recording of muscle length and tension in the muscle spindle and tendon organ, respectively, and pressure detection in the circulation etc. Since most development regarding the molecular aspects of the mechanosensitive channel has been made in nonsensory systems it is important to focus on mechanosensitivity of sensory organs where the functional importance is undisputed. The stretch receptor organ of the crustaceans is a suitable preparation for such studies. The receptor organ is experimentally accessible to mechanical manipulation and electrophysiological recordings from the sensory neuron using intracellular microelectrode or patch clamp techniques. It is also relatively easy to inject substances into the neuron, which also makes the neuron accessible to measurements with fluorescent techniques. The aim of the present paper is to give an up to date summary of observations made on the transducer properties of the crayfish stretch receptor (Astacus astacus and Pacifastacus leniusculus) including some recent unpublished findings. Finally some aspects on future line of research will be presented.

This whole line of thought is ripe for plucking. I guess the function is so intrinsic to each and every cell in each and ever critter that it's all trees and no forest. C'mon researcher guys, give us whatever you come up with. :thumbs_up
Studying humans would be nice.

[Diane]

I think that what the paper (from way back in 2004) shows, is that the brain (in non-CRPS subjects) reveals itself to be more interested in novel stimuli or "threat" potential that comes to it through the face or with social/cognitive ("cultural" or troop?) default diversions, than with interoception or threat-less exteroception further down in the body. I think it's related to what Sapolsky refers to as stress-induced analgesia (p. 194, Why Zebras Don't Get Ulcers).

In this study, particularly finger pads. There is so much hard drive associated with finger pads, why would the sympathetically active part of the brain care about them much at all? Finger tips bits chopped off grow right back in a few weeks.. no big trauma. It's very easy for the brain to keep constant background vigilance over finger tips because of the huge S1 map (which I think reduces its sense of threat about finger tips), and free up a lot of hard drive for the task at hand of monitoring sudden puffs of air or doing mental arithmetic. I see they glued the test finger down.

It's interesting, this paper, but still, it doesn't really help me figure out what effect a skin deep lateral skin stretch on the less-well-S1-mapped portions of the body with non-glabrous skin, has on the nervous system, sympathetic or otherwise, of a completely free-to-move, recumbent individual, who has been asked to sense their breath at their nose and allow themselves to relax.
Maybe I need to read it a few more times.

I'd really like to read the Johansson and Vallbo 1983 paper about skin stretch, increased firing in one axis of stretch and decrease in the orthogonal axis. I will see if it's open access.

Anyway, thank you Luke for digging this one up so I could mentally compost it. :thumbs_up

[Diane]

It looks on brief over view like Johansson and others associated stuck pretty much to glabrous skin, including the foot (http://jp.physoc.org/cgi/content/full/538/3/995). Which is fine.. I found the 1983 paper, which was free access and done on glabrous hand skin. I found it in this long long list (http://www.humanneuro.physiol.umu.se/publications/Tactile.html). At least we know plenty about cutaneous input through hands. :thumbs_up

[Diane]

Here is a link (http://www.somasimple.com/forums/showthread.php?p=41509#post41509) to a paper that discusses the chemistry, evolution, receptors and ligands of mechanosensation in plants and animals, from single cells to multicells. It's fairly long, and alas the pictures do not appear clear. I will have to see if I can bring them here bigger/better.

Apart from the images being small, the paper is one of those that make me glad I was taught to read once upon a time. :thumbs_up

[Diane]

The paper referred to by Luke in post #66 (http://www.somasimple.com/forums/showpost.php?p=41410&postcount=66) where increasing sympathetics by blowing cold air on someone's face unexpectedly or having them do mental arithmetic decreases sensitivity aligns with the findings from the paper "Sympathetic Blockade Increases Tactile Sensitivity (http://www.somasimple.com/forums/showthread.php?t=4520&highlight=Sympathetic+Blockade+Increases+Tactile+Sensitivity)".

[Diane]

I managed to get a blogpost (http://humanantigravitysuit.blogspot.com/2007/11/pain-as-aporia.html) written this morning, about sublation (http://www.google.com/search?rlz=1B3GGGL_enCA226CA227&hl=en&q=define%3A+sublation&btnG=Google+Search). Sublation is an up- or out- lifting, from an apparent impasse, or "aporia".

I love when I learn a new word. My neurons build new bridges, just like ant behavior. (http://www.nytimes.com/2007/11/13/science/13traff.html?ex=1352610000&en=d21a9a2aa82e7116&ei=5088&partner=rssnyt&emc=rss)

[Diane]

I want this great link to Scholarpedia to be available here, in this thread. Mechanoreceptors and stochastic resonance (http://www.scholarpedia.org/article/Mechanoreceptors_and_stochastic_resonance).

Short excerpt: Stochastic resonance(SR) is a counterintuitive phenomenon whereby noise under appropriate conditions can enhance the detection of weak signals rather than interfering with signal transmission. Originally described in nonlinear physical systems, SR is applicable as well for biological processes that are also frequently nonlinear. The article explains SR by using mechanoreceptors to illustrate, and in the process describes a large number of nuances about sensory organs in general and mechanoreceptors in skin in particular. For the skin senses, the primary cutaneous receptors include free nerve endings but more so nerve fibers variously encapsulated to afford specificity and/or amplification.

The article links to this page on stochastic resonance (http://www.scholarpedia.org/article/Stochastic_resonance) in general.

I'm not sure why the author didn't include Ruffini endings in his list. They are the slow adapting mechanoreceptors (http://en.wikipedia.org/wiki/Mechanoreceptor) in skin that look and act like Golgi tendon organs, continuously firing with lateral stretch.

[Diane]

I've been out having internet fun on my day off. From the article above, I noted the following:
Hair cell morphology highlights a conservative evolutionary feature of cell biology as it relates to sensory systems. Although the mechanically-gated ion channels are located in the kinocilia... A word I'd never heard of before. Here are pictures of some (http://www.uni-mainz.de/FB/Medizin/Anatomie/workshop/EM/EMKinociliaE.html). Here is a wikipedia page (http://en.wikipedia.org/wiki/Kinocilium) about it. ...somewhat of a misnomer since they lack the complete axoneme... Another new word (http://en.wikipedia.org/wiki/Axoneme). ...of 9 + 2 microtubules... (There's that word again...) ...characteristic of cilia and flagella, the presence of a kinocilium with its ciliary axoneme and polarizing role in directional sensitivity invites comparison with other sensory receptors that feature non-motile cilia. For example, vertebrate rods and cones arise during development as extensions of a ciliary membrane whose invaginations and vesicles form the outer segments containing photopigments. Olfactory cells also feature cilia, the membranes of which contain the odorant binding receptors and G-proteins that initiate sensory transduction. Likewise, modified ciliary structures are characteristic of many primary mechanosensory neurons where dendrites contain the 9 pairs of ciliary fibrils extending from a ciliary base. Indeed, the cilium arose early on in eukaryotic organisms as a cellular compartment for sensing the environment, as in ciliate protozoans where it functions simultaneously as a sensory antenna and locomotory organelle. For example, a mechanical stimulus applied to the anterior cilia of Paramecium triggers a spike-like membrane potential and calcium current that reverses the effective stroke of ciliary beating resulting in reversed swimming.

docartemis wrote something in a thread on Neuroplasticity (http://www.docartemis.com/cgi-bin/forum.cgi?fid=06&topic_id=1199916629) awhile ago: The receptors in the inner ear are like the photoreceptors of the eye in that they are not true neurons, since they do not generate action potentials. However, they could still be considered part of the peripheral nervous system. The idea of the tongue electrode is to provide an alternative input to the part of the brain that is getting bad signals from the inner ear.

This reminded me of something I read by Lynn Margulis, about how she thought cilia were endosymbiotic (http://www.edge.org/q2005/q05_7.html#margulis). (Here's something (http://en.wikipedia.org/wiki/Endosymbiotic_theory) about that.) She's probably right - her "dangerous idea (http://www.edge.org/q2006/q06_7.html#margulis)" is that we probably are just one great big bacterial colony.

About microtubules, they seem to be merely ubiquitous parts of cellular anatomy regardless of where the cell parts came from evolutionarily, endosymbiotically or not. There's no evidence (despite Hameroff-Penrose quantum theory) that microtubules do much - maybe they lighten the overall load, kinda like air cells in bird bones, or provide space for organelles to travel within the cell. A cell needs to be able to do that neural 'action potential' thing to count as a neuron or as part of an organism-wide signalling system.

In fact, if we're going to bother immersing ourselves in cellular minutiae/parts, I submit that mitochondria might be more relevant, in that
1. they are (endosymbiotic) parts of cells that provide us with energy from oxygen combustion, and
2. the nervous system uses a disproportionate amount of that particular element.