Autonomic state in pain and correction

[Diane]

Here is a copy of the disussion in the Five Questions (http://www.somasimple.com/forums/showthread.php?t=2404) thread that led to starting this new thread on autonomics:
(From Barrett: )Wonderful discussion.

Jon,

Your link regarding category mistakes is especially relevant. As some of you know, I'm currently in Las Vegas where my family has gathered to greet my son Alex. He's home from Iraq for two weeks and his stories of searching the road for explosives designed to deceive him fit here perfectly. He says, "When you travel the same road every day you just know when something has changed." Isn't examination of the human body similar in many ways?

I'l be writing more about this.

I think much of this issue revolves around discovering and defending an accurate and relevant essential diagnosis. This doesn't require great leaps in knowledge toward medical school minutia. I think it's wise to leave that to the physician, whether or not he or she does it well.

The third question:: What is your autonomic state and how is that related to your breathing pattern?

Thoughts?
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Barrett L. Dorko P.T.
www.barrettdorko.com

Old 20-05-2006, 10:48 AM #43
EricM
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I observe breathing patterns looking at apical vs diaphragmatic excursion and rate. I ask about the presence of cold hands or feet. However, recently at least for me, the clinical answers to this question have been split roughly 50/50 in similar chronically painful states. This makes me think either I may be missing something in my assessment, or that autonomic imbalance may only be relevant to the patient in question. What I might interpret as 'normal' may be abnormal to the patient and thus still have a significant influence on the pain state.

Eric

Old 20-05-2006, 02:32 PM #44
nari
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I think that many patients consider cold hands and feet 'normal' because they have always had cold extremities. However, in someone who feels quite 'normal' ambient temperature in the extremities, an increased sensation of warmth after contact is informative.
Long before learning SC, I noticed that patients in an altered ANS state had high RRs, often around 25-30, and apical. After some diaphragmatic practising, they reported feeling calmer and their RR decreased; sometimes the pain decreased, and other times, not. They usually put it down to relaxing.
Then I worked out that they needed to practise deeper breathing while moving around; this worked sometimes; and if they practised during neurodynamic movements, they noticed the pain less, which I put down to distraction.
Several patients found a significant difference between breath-holding and breathing during neurodynamic movement. Some found it much better to hold their breath (on a neutral chest expansion, not on inhalation) during the movement. I personally find the same thing - but I know I am the only person to think this fact.

Eric, I agree that sometimes the autonomic state may only be relevant only to the patient in question. I have seen some dire chronic pain people who are quite warm despite their 24/7 pain state. Not sure about this.

Nari

Old Yesterday, 06:52 AM #45
Barrett Dorko
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Nari,

I would say that my experience of this has been remarkably similar to yours.

Hidden within each of the "five vitals of pain" that lead to the questions is something most evaluative schemes do not have: opportunities to teach and learn along with an obvious relevance. Because of this, a great deal of care is provided during evaluation. This certainly shortens the time necessary to treat people. It'll probably cost the therapist money as well. Too bad.

Cooling in relation to those physiologic and behavioral processes that accompany sympathetic increase is the "physiologic signature" of the abnormal dynamic. I know that there are patients who aren't cold and should be but typically they're good diaphragmatic breathers for some reason, most commonly chior or yoga. In any case, this third question gives me the opportunity show them how these things relate to their discomfort and thus draw them further toward a realization that much of their pain is a consequence of their behavior - behavior they can control.

Abnormally warm people are also out there. Most of the time they have mid-thoracic issues and, I presume, are dysautonomic. I've seen this improve dramatically coutless times. I have no way of proving that of course, so I make no claims.
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Old Yesterday, 07:51 AM #46
Diane
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Lately I treated a woman who is one of the warm ones. She even said, "My feet get so hot that they burn.. I strap ice packs to them so I can go to sleep." She certainly had lots going on between the blades...

The autonomic system has always flummoxed me. I've never understood it well enough to be able to convince myself I can predict what it can/will do, or that anyone else who sounds like they have it down pat, really does. And I've never believed that popping backs somehow enhances or normalizes its function.

I've just acquired another Burnstock book, called Comparative Physiology and Evolution of the ANS.. Haven't started it yet.. if I can make head or tail of it, I'll let you know. All I know right now is that in lots of different species including our own, autonomics make skin change color and hair lift up. Also that skin has ten times the amount of blood flow it needs for its own maintenance, so it can be a metabolic heat radiator/entropy radiator. Meanwhile, for pain, I think it's safe to say that producing any kind of change in autonomics into the opposite direction of wherever they seems stuck, is beneficial. Maybe the rule could be, if it's cold make it warm, if its hot, make it cool.

The other big clue I got was finding out not that long ago that autonomics do the opposite thing in the skin than they do in muscle. I'm still composting that. It's so big that it's taking quite awhile.. it makes sense that the blood shunting mechanism would be different for mesoderm than for ectoderm and endoderm, thinking embryologically. It makes me more convinced than ever that skin is the key to the mansion, not only for pain diminishment but also for autonomics.. just trying to work out why and how.
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Diane


Old Yesterday, 08:48 AM #47
Jon Newman
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Hi Diane,

You may be interested in the following. This is a side bar and if anyone wants to discuss it further maybe a new thread can be started. The current one has a good flow right now but I do think this is pertinent to the discussion.

One of the poster presentations at the APS conference was titled Skin potential as a measurable correlate of moderate to severe chronic pain--a case report and was authored by Donald D'Angelo.


Introduction

There exists a perceived need for an objective measure of pain and pain relief. There is a device used in veterinary medicine to perform bilateral measurements of the electric charge of the skin, skin potential (SP). SP can be used to detect distinctive asymmetries caused by the autonomic nervous system as it responds to moderate to severe persistent pain. SP can accurately reflect changes in the ANS. The goal of this study was to determine if this device might reliably assess pain in humans.

While the methods and results are certainly important, I will simply summarize as this is 'only' a case study. The measuring device is trademarked as PainTrace manufactured by Biographs LLC, Bayville, NY. Here's a quick summary of what they are measuring:

If both palms produce equal voltage, the linear trace will be a flat, horizontal line down the center of the graph paper. We take this line as the X axis of our graph, with the arrow of time to the right. This functions as a neutral baseline with a value of zero. When the right palm is producing higher SP than the left, the linear trace will be above the neutral baseline on the graph. When the right palm is producing lower SP than the left, the linear trace will occur below the neutral baseline.

The picture they show is simply a nickel sized electrode placed in the palm of each hand with the leads running to a chart recorder.


The asymmetrical SP can be accounted for by the ANS innervation of the skin. It has been found in numerous mammalian species that an autonomic response is demonstrated with persistent pain. At the onset of acute pain, the ANS raises sympathetic tone and accordingly blood pressure and heart rate, which have been shown to normalize with respect to time. The activation of baroreceptors by elevated BP, triggers an increase in vagal tone in an attempt to restore homeostasis. This increase in vagal tone has been demonstrated to provide an opioid-mediated partial anti-nocicipetion in both animal and human models. The primary pathway for this effect is mediated via the right cardiac vagal trunk. In addition to the heart, the vagus affects other physiologic changes including a lowering of SP. Thus, during moderate to severe chronic pain, skin on the right side has a lower SP than on the contralateral side, while mild pain fails to trigger the baroreceptors and therefore does not produce changes in SP. After pain relief, vagal tone moves back towards normal, with a coincident fall in SP on the right side.

This D'Angelo fellow by the way is an MD working for New York Harbor VA medical center in the dept. of anesthesiology.


Summary: In all five sessions for this individual, SP was lower on the right side during moderate to severe chronic pain (VAS 4-10). After pain relief, SP on the right rose. Distinguishing between painful and pain-free states in this patients was as simple as seeing whether the trace was above or below the neutral baseline.

It will be interesting to follow whether this technology, if validated, comes into play in future pain studies.

Old Yesterday, 09:08 AM #48
Diane
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Thanks Jon.

At the onset of acute pain, the ANS raises sympathetic tone and accordingly blood pressure and heart rate, which have been shown to normalize with respect to time. The activation of baroreceptors by elevated BP, triggers an increase in vagal tone in an attempt to restore homeostasis. This increase in vagal tone has been demonstrated to provide an opioid-mediated partial anti-nocicipetion in both animal and human models. The primary pathway for this effect is mediated via the right cardiac vagal trunk. In addition to the heart, the vagus affects other physiologic changes including a lowering of SP. Thus, during moderate to severe chronic pain, skin on the right side has a lower SP than on the contralateral side, while mild pain fails to trigger the baroreceptors and therefore does not produce changes in SP. After pain relief, vagal tone moves back towards normal, with a coincident fall in SP on the right side.
It still doesn't make sense yet. In other words, I still can't quite "see" it yet. I see a vague random rise and fall, sort of like the sea heaving around but I can't make out what is calming it down and what is making it rise. My confusion is directly proportional to the lack of focal length/ability to see a big(ger)/ the big(gest) picture, and was based originally on a category mistake named "peripheral/central" instead of "ectodermal/mesodermal/endodermal".

Other thoughts/beliefs I've held about the ANS that need closer looking/ deconstruction:
1. parasympathetic good for pain, sympathetic bad for pain
2. touching improves parasympathetic function
3. exercise increases sympathetic function
4. autonomics are essential for breathing, digestion, heart function
5. that there must be consistency somewhere in it that I'm missing (maybe there isn't any consistency or fixedness or predictability, maybe there is only perpetual dialectic)

Definitely, let's start a new thread. (I started one awhile ago.. can't find it just now.. I posted a picture of an interneuron. The thread died and got lost. I'll repost the picture.)
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Diane


Old Yesterday, 03:36 PM #49
Barrett Dorko
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A new thread about the autonomic state in pain and during correction sounds good. To me, it's the least well understood portion of the "five vitals" equation. Jon's attendance to that conference is really paying off for all of us here.

Time for the fourth question : Which ways do you want to move and how does that make you feel?

I always ask my classes at this point - How do I ask this question?

Any takers?
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Barrett L. Dorko P.T.

[emad]

Diane,thanks for setting this new thread for ANS ,it is worth as it is directly related to the severity or degree of pain in most of the patients we encounter and i think it is direct relation between the psychological and physical matters of the body .

Regards
Emad

[Diane]

You're welcome Emad.:)

While I was doing a comparison between Grieve's 2nd and Grieve's 3rd editions of Modern Manual Therapy, I re-discovered Chapter 20 in the 2nd ed, by Grieve, called "The autonomic nervous system in vertebral pain syndromes".
Apart from the juxtaposition of the words "vertebral" and "pain" (as in the adjective vertebral modifying the noun pain, as if the mesoderm were largely respoonsible for back pain..) the article is a run down of the ANS up to 1994.

Here is a summary, paragraph by paragraph. The intro starts with a quote from Lewis Thomas in 1984:

INTRO:
The greatest difficulty in trying to reason your way scientifically through the problems of human disease is that there are so few solid facts to reason with. It is not a science like physics or even biology, where the data have been accumulated in great mounds and the problem is to sort through them and make connections on which theory can be based.

Alrighty then..
Paragraph 1:
- nervous system is a continuum, word "autonomy" (from Langley 1898) is misleading, suggests it works in isolation;
- Williams et al (1989); although connections with somatic elements not always clear, evidence exists for visceral reflex activity stimulated by somatic events including trauma;
- term "PNS" includes cranial, somatic visceral and splanchnic nerves (Fig. 20.1-20.5); better term is "involuntary"

2.
- autonomic and somatic divisions originate together from same basic units or neurons (her doesn't name neural crest specifically but that's where they come from) associated in similar reflex arcs; related structurally and often closely connected (Mitchell 1954);
- somatic and autonomic parts are more alike than different;
1. The essential morphology and arrangement of afferent neurons is similar in somatic and visceral systems, yet it is incorrect to speak of 'afferent autonomic neurons' since the symp and parasymp systems are purely 'outflow' systems and are thus entirely efferent (Wyke 1990). The phrase 'visceral afferent neurons' is employed by Williams et al (1989).
2. The dorsal spine roots convey afferent traffic from soma and viscera alike; the dorsal spinal ganglia contain nerve cell bodies of visceral as well as somatic afferents.
3. It has been shown (Pomeranz et al 1968) that the small-fibre nocioceptive afferents from both somatic tissues and viscera converge in the substatia gelatinosa cells. Somatic and visceral afferent fibres conveying nocioceptive impulses have the same histological appearance, being mainly unmyelinated neurons with diameters of 0.2-1.5 um (although some somatic nocioceptive afferents may be up to 4.0 um in diameter) (Williams et al 1989).
4. There are further similarities between the two systems in that axon reflexes can be elicited at terminals of autonomic postganglionic fibres (Williams et al 1989).
5. The phenomenon of peripheral axonal sprounting occurs in sympathietic nerve fibres as in somatric nerves (Shafar 1966).
6. Degenerative changes in the autonomic system are the same as in the somatic system (Williams et al 1989). After injury, autonomic nerves demonstrate great regenerative capacities (Brodal 1981).


- "Musculoskeletal pain and associated symptoms cannot be considered in isolation from concomitant changes in autonomic neuron activity."

SOMATOVISCERAL/VISCEROSOMATIC REFLEXES
paragraph 1.
- Gaskell (1961) proposed studying ANS in terms of reflexive behavior;
2.
- list of researchers between 1945 and 1978;
3.
- segmental innervation, Head 1920
4.
- facilitated segment, Denslow et al 1947
- Kostyuk confirmed relation at the posterior horn 1968, showed "afferents from viscera can cause presynaptic inhibition upon somatic afferent impulse traffic" and also "exert postsynaptic inhibition which is under supraspinal modulatory control from the bulbar reticular formation."
- Pomeranz et al 1968 showed that "visceral afferents inhibit the effect of converging afferents from the skin and conversely, stimuli to the skin can cause inhibition of neurons on which visceral afferents terminate."
- same mutual inhibition is exhibited by group III afferents from skeletal muscles and skin.
- thicker neurons penetrate deeper into dorsal horn, as a rule;
- unmyelinated Cs terinate in laminae I and II;
- some small myelinated A-deltas may get as far as layer V;
- large myelinated cutaneous afferents get to III, IV, and V;
- largest sensory aferents from muscle reach lamina VI.

5.
- laminae I and II are major layers for nocioceptive reception;
- "nocioceptive collaterals in deeper layers are polysynaptic and are active in initiating visceral and somatic efferent traffic, producing changes in autonomic function and skeletal muscle as a consequence of nocioceptor input."

6.
- nocioception from viscera travels in splanchnic nerves, probably enters spinal cord via white rami communicantes and dorsal spinal roots; then evidence suggests it occupies the lateral spinothalamic tract (Williams et al 1989);

7.
- collaterals of the ST tract recruit more autonomic activity, relay it through the periaqueductal grey matter to nuclear cuneiformis and on from there to hypothalamus;

8.
- viscera insensitive to cutting, burning or crushing, but react to excessive tensioning; referral cutaneously is common; once peritoneum becomes involved, e.g. inflammation, spasmodic pain in the region results;

9.
- painful skin area/referrral zone "acutely tender", "cutaneous vasoconstriction" may be evident;

10.- "Conversely, pain unaccompanied by a greater or lesser degree of visceral reflex activity, e.g. one or more of changes in pulse rate, blood pressure, vasomotor and temperature changes, sudomotor activity and pupilliary diameter, has not been described."

11.
- autonomic reflex activity not initiated solely by general visceral afferent pathways;
- "In most instances demanding general sympathetic activity for effort, the afferent element is usually somatic, from the special senses or the skin. Rises in heart rate, blood pressure and pupillary dilatation may result from somatic receptors in the skin and other tissues. Conversely, contraction of the muscular abdominal wall - a somatic structure - often results from irritation of abdominal viscera. Also, axon reflexes may be evoked by stimulation at the terminals of autonomic postganglionic fibres (Willams et al 1989)." (emphasis mine)

More to come. Next, Musculoskeletal pain and concomitant features.

[Diane]

Musculoskeletal pain and concomitant features
Paragraph 1:
- all the symptoms evoked by spinal joint nocioception.. "All were relieved of these symptoms by manual treatment to the T5-6 segment and adjacent structures." (pallor, sweating, bradycardia, fall in BP, feeling of faintness, nausea..)
2.
- familiar experiences, borborygamous provoked by mobe- ing T5 in prone patient, cold sciatic leg, etc.. (shopping list of autonomic states connected to spinal manual therapy or stress of T spine... no mention of any other sort of treatment or of another location initiating autonomic changes)
3.
- confusion from tenderness of abs.. easily referrred pain from T spine..
4.
- myofascial "trigger points" mentioned.. thought to be capable of disturbing visceral function -> somatovisceral
5.
- viscera can refer to skin and also to skeletal muscle -> activate trigger points..; "myofascial pain may initiate vascular changes, e.g. variation of skin temperature, reddening of cunjunctiva and secretory changes like coryza, lacrimation, localized sweating and pilomotor changes as 'gooseflesh'."
6.
- facial pain..close association of trigeminal nerve with autonomic ganglia.. more about trigger points.. mention of idea of vertebral joints affecting visceral conditions being a tad outdated..
7.
- mention of former notions of manip as "soverign remedy for all ills, visceral as well as musculoskeletal"

SO-CALLED AUTONOMIC PAIN
Paragraph 1
- various coined and arbitrary classifications of pain
2.
- the phrase "autonomic pain" "may be attractive"..
3.
- how electric/mechnical stim of various sympathetic ganglia has led to pronounced pain states/anxiety
4.
- Nathan 1976 -> "refers to visceral afferent fibres conveying both visceral sensation and pain. Whether this is called 'autonomic pain' seems a matter of semantics."
5.
- local anaesthetic into sympathetic nerves to treat neuralgia of ulnar nerve
6.
- drawback: if term such as 'autonomic pain' is proposed, another term like 'somatic pain' follows, and then differences must be drawn.. besides, autonomics are efferent.
7.
- Bogduk 1983 -> reviewed clinical features of causaligia and RSD, said that "in sympathetic pain syndromes affecting the limbs, the mechanism of pain lies in the somatic and central nervous systems - 'whatever sympathetic features occur are only epiphenomena superimposed on this pain.' "
8.
- Melzack and Wall (...finally!); fibre diameter not enough, may be completely irrelevant, in explaining origin of pain in neuropathies;
- sympathetic effector neurons have crucial role in exciting somatic afferent sensory fibres, idea originally proposed by Richards 1967..;
- e.g. nerve injury, neuroma forms after nerve transection;
- axon sprouts "show marked spontaneous ongoing activity without apparent stimuous"
- sensitive to noradrenalin whether applied directly or in blood vessels supplying the neuroma (See AIGS thread);
- "A mixed nerve inevitably contains sympathetic efferent fibres, and since new axon sprouts a temporarily devoid of the tubular insulating myelin sheath small numbers of adjacent neurons begin to excite each other i.e. ephaptic transmission (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6255143&dopt=Abstract) or 'cross talk between fibres' (Melzack and Wall 1982)."
- "Thus sympathetic neuron effector traffic, at the site of injury, is transposed to adjacent afferent neurons as sensory stimulation. This superimposed afferent traffic reflexly triggers even more sympathetic neuron output, so that the limb is not only painful but glossy and moist."
9.
- discussion of the drug guanethidine, persistent pain, central pain... "Perhaps the phrases 'autonomic pain', 'sympathetic pain', or 'parasympathetic pain' have about as much validity as the phrase 'somatic pain', perhaps there is only pain, with the inescapable degree of autonomic reflex activity sometimes overwhelmingly and disasterously to the fore."

Next: THE POSSIBLE BASIS OF SOME CLINICAL FEATURES

[Jon Newman]

I'm getting close to wrapping up some of the things I learned at the APS conference this year but I've got a few things left. I went to a lecture titled "Cardiovascular and pain regulatory system interactions: Implications for hypertension risk and chronic pain." I figured this was the best place to hear something about the ANS and pain. Unfortunately I'm not that much clearer on the topic partly because I don't have a deep enough understanding to appreciate all that was being covered and partly because it is so complex, even for those whose career is centered on the topic. But I'll try to add some things I found interesting. I'll add the thoughts of three different presenter's in three different posts. First up, Christopher France (http://www.psych.ohiou.edu/people/faculty/france/france.html) discussed "Hypertension, risk for hypertension and pain".

Apparently hypertension and risk of hypertension are associated with hypoalgesia. They found decreased pain in humans with hypertension(HTN) during electrical tooth pulp stimulation, thermal stimulation and mechanical stimulation. They also found that normotensive individuals at risk for HTN (e.g. parental history, current high blood pressure) exhibit hypoalgesia.

He presented information that demonstrated that the hypoalgesia present in individuals with HTN or at increased risk for HTN does not appear to be mediated by enhanced endogenous opiate activity--this theme was reiterated through all lectures.

Something mentioned only in passing during the lecture but which I found very interesting is that once someone knows they are hypertensive they are no longer hypoalgesic. I'll try to tie in some autonomics in the next post.

[Jon Newman]

The next speaker was Mustafa al'Absi (http://www.d.umn.edu/~malabsi/mustafa.htm) whose presentation was titled "Adrenocortical responses to opioid blockade in hypertension prone men and women."

I'll provide some "bullets" from his powerpoint presentation much of which builds on my last post and ties in with my next (whenever that happens).

--Pharmacologically increased PB reduces pain avoidance.

--The presence of adrenal steroids varies directly with hypertension risk in animal models of hypertension

--Enhanced activation of autonomic controlling centers of the hypothalamus and medulla in individuals at high risk for HTN.

--Enhanced sympathetic and hypothalamic-pituitary-adrenocortical (HPA) axis activity

If I understood correctly endogenous opiates have an inhibitory effect on cortisol response in terms of timeline--Specifically cortisol levels increased following pain assessment after the ingestion of naltrexone, but not placebo. The low HTN risk group exhibited an earlier peak of cortisol response.

Lastly, he reiterated that hypoalgesia in HTN-prone individuals does not appear to be mediated by enhanced endogenous opiate activity.

I've got some references for "suggested readings" from all the presenters if anyone is interested.

[Diane]

I've got some references for "suggested readings" from all the presenters if anyone is interested.

Some new/recent references would be great!

Thanks for adding your posts. This thread will likely be more a repository than a discussion.. which is just fine.. a space for spreading out inventory before decluttering/doing a yard sale.

[stregapez]

So, do cold hands and feet often correspond with sympathetic activation? And do they often correspond with high blood pressure? Am especially curious, as , like i sad, I have sort of cool-prone hands (mostly the right one lately), and used to have cold hands /feet. Have always had low (low-normal) blood pressure. According to a saliva test done a year 1/2 ago, and a pharmacist who interpreted it, I have low cortisol levels too. No idea what that means. He suggested they were possibly depleted "from stress," and another pharmacist who worked in the same place tended to disagree and suggested it's because I am "laid-back." Me, I can never figure out if I am very laid back or just totally stressed :)

Dana

[Diane]

THE POSSIBLE BASIS OF SOME CLINICAL FEATURES
1. Dissemination and amplification of autonomic effects
2. Cranial symptoms after cervical injury of secondary to upper cervical arthrosis
3. Musculoskeletal changes as lesions of trespass
4. Autonomic nerve involvement in referred pain and other symptoms

The rest of the chapter is the elaboration of these 4 points, and a bunch of diagrams, which I will bring later.

Here is another thread that died a premature death, on the topic of autonomics (http://www.somasimple.com/forums/showthread.php?t=2348), which features a depiction overall.

[emad]

Diane ;

Good topic .

#
You or the writer you copy from back again the concept of Trigger
points ,which since at least 3 years i had begun to put it behind ,because
of lack of scientific evidence .

#
Seems you or Jon copy views of medical schools whom sometimes i believe
they look at pain issues as arthrosis ,arthiritis ,systematic ,,joints ,,,,.For
example ,most of cervical cases they look at as cervical spondylosis .

#
In general,the topic is very interesting as it discuss a feature of pain cases which we usually we meet as patient,s complaints .

Regards
Emad

[Diane]

Good points Emad.
You or the writer you copy from back again the concept of Trigger
points ,which since at least 3 years i had begun to put it behind ,because
of lack of scientific evidence . Agreed. Apparently Grieve was still thinking about them in 1994 when this text came out, along with lots of other mesoderm.

[Diane]

Page 297:
1. Dissemination and amplification of autonomic effects
When examining and treating patients, reliance on the classical anatomical facts of autonomic nerve arrangement, and the older physiology of neural traffic in autonomic ganglia and at effector endings, may be insufficient in terms of appreciating the possible basis of clinical features. I like this.. it signals humility in the face of a fractal nervous system.
Structural and functional examples of dissemination and amplification of autonomic effects

Structure
The classically-described distribution of autonomic nerves is sketched in Figures 20.1 - 20.5, yet the segmental levels of outflow for sympathetic efferent neurons (Johnson & Spalding 1974, Williams et al 1989) are not universally agreed. Some authors place the sympathetic supply to the heart beginning as high as C3 (Lindahl & Hamberg 1981). Continental anatomists (Tinel 1937, Laruelle 1940, Guerrier 1944, Delmas et al 1947) reported the cell bodies of preganglionic sympathetic neurons in the cervical segments C5-C6-C7-C8 and joining these somatic roots, although many give the uppermost as T1. The French authors stated that the rami communicans from these neurons also mank synaptic junctions with the small sympathetic ganglia developed around the vertebral artery in the foramen transversarium between C4 and C6.

On the other hand, Bogduk (Ch.22) observes that 'the so-called "vertebral nerve" consists of no more than grey rami communicantes accompanying the vertebral artery - stimulation of these nerves in the monkey failed to influence vertebral (artery) blood flow.'

Variations, between a purely preganglionic and postganglionic arrangement, are described. In addition to white and grey rami, mixed types occur. In the cervical region, bundles of thick myelinated fibres join the grey ramus to reach the prevertebral muscles, and at thoracic segments grey and white rami may be fused (Williams et al 1989).

Day (1979) mentioned that it is difficult to state precisely the source of all the nerve fibres (particularly sympathetic) supplying a given tissue.

Peripherally, the extent of segmental areas innervated is variable. There is considerable overlap of supply by adjacent nerves. The innervation by different effector systems, e.g. vasomotor and sudomotor, of a particular nerve are not necessarily the same. Textbook descriptions of autonomic innervation differ considerably. There are special differences, as well as variations between individuals.

Schemes such as these shown in Figures 20.1-20.5 are no more than simplified summaries. It is probable that the full detail of distribution is much more complex. Williams et al (1989) allow the possibility of a limited outflow of preganglionic fibres in other spinal nerves, and mention the certainty that 'nerve cells of the same type as those in the lateral grey column also exist at other levels, above and below the thoracolumbar outflow (Mitchell 1953), and that small numbers of their fibres issue in corresponding ventral roots.' Operative findings indicate that many individuals do not have a symmetrical arrangement to the upper limb, and it is known that prefixation and postfixation occurs, as in the somatic limb plexuses (Johnson & Spalding 1974). Increasing deterioration of autonomic nerve function in ageing reflects the increasing occurrence of Wallerian degeneration and segmental demyelination. Regeneration does not keep pace with successive degenerative events. Appenzeller and Ogin (1973) suggested that functional deterioration may in part be attributed to changes in the myelinated fibres (white rami communicantes) of the paravertebral sympathetic chain.

Is it any wonder we get so confused about how this works when it is structurally, anatomically, and behaviorally so variable?
Next, Function.

[Jon Newman]

Here's one article (http://hyper.ahajournals.org/cgi/content/full/41/6/1228) Diane, as I've stated, the information is confusing--at least to me. Sticking with the confusion theme I'll add some thoughts from the last presenter. While the first two presentations focused on hypoalgesia in HTN, the last presenter, Ok Yung Chung (https://medschool.mc.vanderbilt.edu/brain_institute/php_files/faculty_blurbs.php?ID=1806) looked at whether chronic pain is a risk factor for HTN. Here's some highlights

Chronic pain as a prolonged stressor can:

--elevate blood pressure and increase the risk of cardiovascular disease by stimulating the sympthethic nervous system

--result in slower recovery from the release of adrenal hormones


--Healthy controls show effective opioid modulation of SBP recovery and return to baseline following acute pain stressor

--Chronic pain patients do NOT return to baseline and show NO opioid modulation

Sympathetic nervous system in HTN

--contributes to the initiation and maintenance of HTN
--SNS activity is heightened by impariment of cardiovascular reflexes (baroreceptor reflexes)
--Causes vasoconstriction
--Enhances sodium retention
--creates trophic effects on blood vessels
--results in abnormalities in ion transport

I've got to stop now but next up is "Links between pain pathways and the autonomic nervous system"

[Diane]

Thanks Jon.
More please.
One thing that can be said about the autonomics that I forgot to mention in my little list way back when, is how related their function is to cognitive/social/emotional states. They are like ideomotor movement that way.

Here are thumbnails from the Grieve's article.

[Jon Newman]

While pinning down the interaction of the ANS and pain is confusing it perhaps isn't nearly confusing as my lead in sentence to my last post. Hopefully what follows is written more coherently.

More bullets from Ok Yung Chung

--Common anatomic sites exist for the generation of both HTN and chronic pain

--This "central autonomic network" controls and coordinates visceromotor, neuroendocrine, pain, and behavioral responses essential for adaptation:

Insular and prefontal cortices
Amygdala
Hypothalamus
Periaquaductal grey (PAG)
Parabrachial region
Nucleus tractus solitarius (NTS)
Ventrolateral medulla (reticular zone)

I kept in the anatomy part just to be thorough, not because I actually know where all this stuff is exactly (and also so the following makes more sense).

Pain and blood pressure: reciprocal process

Increased BP-->Baroceptor activation-->Activates NTS-->Inhibits rotral ventral medulla-->increased descending pain inhibition and decreased SNS outflow-->decreased BP

Depressed baroreflex functioning may be due to dampening of the sympathetic inhibitory centers (NTS) and preservation of centers that exert a positive modulation of sympathetic tone (rostral ventromedial medulla or RVM)

Maybe those semesters in neuroscience were important after all. If I'd only paid attention.

Links between pain pathways and the ANS

--Vagal baroreceptor afferents to the NTS send descending afferents to the autonomic centers of the spinal cord

--The hypothalamus coordinates autonomic and sensory information, including ascending spinal nociceptive signals, and elicits antinociception via links to the NTS, PAG, and RVM (NRM) which ultimately trigger the activation of descending noradrenergic pathways.

--The medial preoptic nucleus projects to the PAG and the RVM. It has an important role in the autonomic response to pain.

--The brainstem locus coeruleus:

Provides norepinephrine to all major levels of the neuroaxis including cardiovascular regulatory areas (e.g. ventral medulla, NTS) and pain inhibitory areas (e.g. NRM via alpha-2 adreneric receptors)

Integrates afferent information from the baroreceptor centers and the limbic system, thereby influencing sympathetic tone.

--The amygdala is a critical region for mediating the expression of autonomic, neuroendocrine, and behavioral changes that occur in response to fearful or aversive stimuli, such as pain.

I don't know about you but that's enough for right now. This particular lecture was full of interesting info. There is more pathway type information (specifically, opioid system and the RVM and Adrenergic system and the RVM) that I suppose I can provide if people are dying to know but otherwise I'll try to capture some other interesting factoids that I feel may be pertinent and post them in my next entry.

[Diane]

Jon, give us everything you've got. As long as your fingers hold out. And including the anatomy would be really good.

Function
The presence of intermediate sympathetic ganglia (Boyd 1957), and independent sympathetic connections, implies a multiplicity (Erhlich & Alexander 1951) of neural pathways much richer than classically described (see also fig. 20.12). Some 50 years ago, van Buskirk (1941) described ascending sympathetic neurons from as far caudal as the seventh thoracic segment. He quotes the work of Smithwick (1936) who reported that complete sympathetic denervation of the upper extremity in the monkey, by section of the anterior roots of thoracic nerves, requires section of all the roots down as far as the twelfth thoracic segment.

The earlier concept of autonomic ganglia as mere relay stations has been much broadened by work in the fields of electron microscopy, neurohistochemistry and electrophysiology (Williams et al 1989).

The variety of neuron types in autonomic ganglia is known to be much greater than previously implied by the simple, dualistic terminology of 'preganglionic' and 'postganglionic'. In the superior cervical sympathetic ganglion, the ratio of preganglionic to postganglionic neurons may be 1:175, for example (Ebbesson 1968). There are wide variations in individuals of the same species (Gabella 1976), e.g. from 1:63 to 1:196 in man - a substrate for the wider dissemination of sympathetic effects than a simple 1:1 relationship. This characteristic is not exhibited to such a degree by parasympathetic ganglia. New knowledge also suggest the phenomenon of amplification of sympathetic effects, and mechanisms underlying this characteristic may be (a) widespread terminal arborization of preganglionic neurons, (b) the mediation of interneurons, (c) the paracrine effect, i.e. intraganglionic diffusion of loically produced transmitter substances and/or endocrine effect, intraganglionic diffusion of substances conveyed from elsewhere.

All of these mechanisms may amplify effector activity.

Next, vascular channels, synapses, and interneurons. All this is still under point 1., Dissemination/amplification.

[Jon Newman]

Alrighty then, for Diane (still info. provide by Ok)

Opioid system and the RVM:

--The RVM receives its major inputs from the midbrain structures, PAG and culeus cuneiformis, and from the limbic and prelimbic cortex.

--The PAG and RVM contain opioid receptors and the PAG-RVM connection is critical for both pain modulation and integration of autonomic and somatic reactions, including the baroreflex.

--There are three distinct populations of neurons in the RVM
ON cells (facilitate nociception)
OFF cells (inhibit nociception)
Neutral cells (no consistent change)

--REVM OFF cells are activated and ON cells inhibited when mu-opioid receptor agonists are given systematically in the PAG or directly in the RVM.

Adrenergic system and the RVM

--The RVM receives dense catecholaminergic innervation. The locus coeruleus (A6) and the medullary pontine cell groups (A1, A2, A5, A7) are the hypothalamus, thalamus, and spinal cord.

--The noradrenergic system does not appear to be tonically active. Noradrenergic neurons may be recruited by activation of the PAG or RVM.

--Norepinephrine has opposing effects at alpha-1 and alpha-2 receptors, with alpha-1 agonists facilitating, and alpha-2 agonists inhibiting nociceptiv transmission.

I'll add other, perhaps more digestible, information later. If I'm not back in five minutes... just wait longer.

[Diane]

You're a funny man, Jon..:star:

(Still under 1. Dissemination and amplification of autonomic effects: )
Vascular channels:
The vascular connective tissue stroma of ganglia is linked to perineural spaces by minute channels, possible avenues for movement of neurotransmitter and hormone substances between neurons, and between these and blood vessels. Aha.. the ganglia is a leaky boat. That makes sense; if a ganglia is a place that processes regional information (like a big pre-brain chat room) it makes sense that it would be as communicative within itself as it could possibly be, through interconnectedness and neuro"chemically".
Synapses:
In the nervous system as a whole, synapses between neurons involve the junction of almost any part of the neuronal surface. Electron microscopy reveals many types, classified by neuronal processes involved or direction of transmission, e.g. the most frequent axo-dendritic, the quite common axosomatic, and also axoaxonic, dendroaxonic, dendrodendritic, somatodendritic and somatosomatic types. Everyone got that? Anything neural can touch anything neural and make a synapse apparently.
The terms reflect the morphology of the junctions. Axodendritic and axosomatic synapses are found in autonomic ganglia (Williams et al 1989). While axosomatic synapses are lerss numerous, sympathetic ganglion neurons reveiver great numbers of axodendritic synapses from preganglionic fibres, forming several synapses with numerous separate dendrites - perhaps representing the mechanism for dissemination or amplification or both. The mode of termination of preganglionic axons is highly variable (Brodal 1981). It doesn't say, but I'm guessing that means, from one individual to another..

Interneurons:
Most ganglion cells are large (25-50 um diameter) and multipolar. Smaller and less numerous cells (15-20um), clustered in groups and less multipolar in shape, have been identified in sympathtetic ganglia and are probably interneurons. These 'small intensely flourescent (SIF) cells (Evanko 1978) contain catacholomine neurotransmitters, their supposed action being the release of dopamine which unites with the surface receptors of ganglionic neurons and modifies impulse transmission patterns. Types I and II SIF cells have been described, and there is evidene that type II cells pass their secretions into local blood vessels (see above), thus exerting more diffuse and distant effects.

Brodal (1981) mentioned the many unsolved problems relating to structure and functional organization of autonomic ganglia.

I found lots there to satisfy my appetite for anatomical minutiae. Plus I'm starting to think we should get whatever this Williams person was busy doing in 1989, since most of this chapter seems to derive from it.
Next is point 2., Cranial symptoms after cervical injury or secondary to upper cervical arthrosis.

[emad]

Diane & Jon :

The last posts are so academic ,thanks for posting , i try to survey as possible , i read what i like or interested in .

Anyway , i liked the last image ,but it is too small , i can not enlarge it , i hope bernard reads me now to find what we can do , i download it but can not read around the image .

Regards
Emad

[Diane]

2. Cranial symptoms after cervical injury or secondary to upper cervical arthrosis

Long section, notes only.
paragraph 1.
- Barre-Lieou syndrome from 1926; headache, vertigo, tinnitus, ocular problems;
- was found in conjunction with cervical arthrotic changes;
- more prevalent with increase in MVAs especially rear-enders; neck pain more common after rear impact (84%, Deans et al 1986);
- the shorter the impact time the greater the rate of change of velocity or acceleration;
2.
- "Injury to the cervical spine is almost without exception due to indirect violence (von Torklus & Gehle 1972), the force being applied to head or rmp and the neck sustaining a considerable proportion of it."
3.
- multiple "sprained ankles" in the neck (lots of mesodermal emphasis)
4.
- headache mechanisms
- injuries on atheletic field
5.
- fall in a shower
6.
- these cases present with one or more of:
-Suboccipital, neck and yoke area pains, unilaterally or bilaterally, with bouts of frontal headache which may be periodic and transient or remain as a dull and constant background ache
- Facial and anterolateral throat pain
- Patches of subjective facial numbness
- Otalgia
- Retro-orbitial pain - sometimes paraesthesiae 'in' the eye
- Subjective laryngeal disurbances, with compulsive clearing of the throat
- Upper pectoral area and axillary pain
- Feelings of instability or dysequilibrium, with sometimes a tendency to list to one side
- Disturbances of hearing and/or vision
- Depression, and feelings of fatigue
- A belief that they are becoming neurotic and 'should pull themselvers together'
- Irritability, insomnia and light-headedness
7.
- Roca (1972); blurred vision, strain, fatigue, diplopia, photophobia, inability to read, anxiety, depression;
- amaurotic episodes, decreased accomodation and convergence, anisocoria, possible vitreous detachment, hyperphoria, hypertropia, ptosis, inability to focus
8.
- Downs & Twomey (1979); symptoms are credible;
- patients tend to move the neck cautiously, apprehensively, seek neutral comfortable positions
9.
- Worth (1985); less sagittal segmental mobility at the OA segment although xrays are normal usually

(long section on radiographic investigation... C4 root sleeves often show defects.. suprascapular region often weakish.. fusions etc. (:cry:) )
Comment: This report is described in some detail because of its salient findings, a consistent involvement of the C4 root sleeve in 'whiplash' syndrome. The findings at myelography and at operation were of lateral 'soft' disc herniations at C3-4, exerting trespass not directly on the spinal cord but on the C4 root and more so the ventral root. The author enlarges upon the C4 root communications with the superior cervical ganglion, via branches of the postganglionic fibres, and suggests that irritation of the C4 root compromises the function of these communications, thus resulting in symptoms related to the sympathetic nervous system. He also mentions, among other observations, that tinnitus might be produced by sympathetic stimulation of the caroticotympanic nerve, and that ocular symptoms may be produced by the aberrant influence of the internal carotid plexus on the ciliary muscles or by reduced flow in the opthalmic artery. Maybe, maybe not.
Again, the connections between the upper cervical nerves with the vagus, accessory, and hypoglossal nerves, through the superior cervical ganglion, have been postulated as the substrate for the cervical spine's ability to produce the synptoms described (Campbell & Parsons 1944, Braaf & Rosner 1975). His explanation of the production of symptoms may be speculative to a degree (see also Grieve 1988), but the segmental identification of a consistently involved nerve root sleeve is a decided step forward in management, whether by surgery or conservative treatment of these distressing syndromes. The rest is all on handling and difficulty of prognosis. Slow recovery, need to be gentle (duh..). No great insights into how to handle, which in his view is all about mobe-ing. Sure. The neck loves that. (not.) Nothing here about how to unload the nervous system/C4 nerve root sleeve, by considering everything that might be affecting it and working from the outside in instead of trying to barrel directly in on it. Oy.

Next, 3. Musculoskeletal changes: lesions of trespass. Some photos of osteophytes that are huge. Think I'll skip them.

[Jon Newman]

Those who can admit to liking Jim Carey might recognize the opening and closing lines of my previous post were borrowed (alright, stolen) from Ace Ventura. Now, more than 5 minutes later, here's some more riveting reading. Any neuroscience profs reading? Please feel free to add your thoughts.

Norepinephrine, a common neurotransmitter for chronic pain and hypertension

--Is released in the spinal cord by acute somatic (noxious) stimuli

--Mediates antinociception elicited by acute induction of hypertension

--Modulates nociceptive information in the dorsal horn prior to its transfer to higher centers

--Is implicated in descending antinociceptive activity elicited by stimulation of the PAG, via a RVM-A7 link in the NRM (got that?)

--Is involved in controlling mood, arousal and attention

Chronic pain and blood pressure regulation

--In healthy normotensives resting BP and pain sensitivity are inversely related

--Resting BP/acute pain sensitivity relationship is altered in chronic pain patients

--Chronic pain patients have a higher prevalence of HTN

--Greater severity of chronic pain predicted presence of HTN beyond the effects of age, race, and family history of HTN

--This fits with "chronic pain as stressor" theory

"Subgrouping" is becoming more popular in the literature and this presentation was no exception. I found the subgroups presented (these are proposed, not definitive) easier to swallow as the subgrouping is based on physiological differences.

Intact Baroreflex

--Postive resting BP/pain sensitivity relationship
--Baroreflex activation by increased BP suppresses SNS outflow but is NOT analgesic due to:

Dysfunction in descending pain inhibitory pathways normally tirggered by BR activation (via exhaustion, dysregulation, loss of downstream responsiveness)

Low-intensity vagal stimulation triggering DF

Greater central/peripheral sensitizaiton, consequent increased pain sensitivity

--Diminished activation of PAG/RVM or opioid receptor desensitization may lead to reduced recruitment of alpha-2receptors and thereby increase pain sensitivity

Imparied baroreflex

--Negative resting BP/pain sensitivity relationship

--Increased sympathetic outflow due to impaired baroreflex modulation leads to analgesia via:

Increased descending pain inhibition through increased alpha-2 adrenergic activation (PAG via RVM and NRM), coerulospinal noradrenergic and raphe-spinal serotononergic inhibitionof the spina cord

High-intensity vagal stimulation triggering DI

Less extensive central/peripheral sensitization

--Impaired baroreflex similar to hypertensives

--Impaired baroreflex increases cardiovascular risk despite association with reduced pain sensitivity in chronic pain

For those craving conclusions, you'll have to wait for one more post.

Above info. still from OkYung Chung's presentation

[Diane]

For those craving conclusions, you'll have to wait for one more post.
Alrighty then.

[Jon Newman]

Conclusions from Ok.

--Chronic pain patients display imparied post-stress BP recovery and opioid BP modulation, and have a higher prevalence of HTN

--A subset of chronic pain patients may have a major impairment of baroreceptor ability to restrain sympathetic tone leading to HTN and eventual end-organ damage, such as CHF

--Untreated severe chronic pain via sympathetic stimulation and impaired barorefelex could increase risk for MI.

--The combination of sympathtic predominance, vagal withdrawl, and blunted baroreflex sensitivity in some pain patients may represent a treatable mechanistic link between chronic pain and future HTN

--Blood pressure related anti-nociception may be due to descending inhibitory influences from overlapping brainstem sites involved in cardiovascular regulation and pain modulation

--BP increases resulting from acute sensory or emotional excitation may trigger CNS dampening that augments vagal and sympathoinhibitory negative feedback mechanisms to help restore safer BP levels.

--Afferent input from the aortic depressor nerve may exert a tonic inhibitory influence on nociception that is enhanced in hypertensive animals and depressed in chronic pain individuals with lower baroreceptor sensitivity

--Animal studies support central mechanisms affecting both BP and nociception versus peripheral causes depending solely on baroreceptor input.

[Diane]

Before I leave point 2 completely, I'll mention a study done in 1990 by Gargan and Bannister on whiplash, refuting the contention that whiplash pain goes away after settlement of litigation.
(They) reviewed 43 patients who had sustained soft-tissue injuries of the neck, a mean of 10.8 years previously. Of these, only 12% had recovered completely, with residual symptoms intrusive in 28% and severe in 12% Only 48% of the group had been wearing seatbelts; 88% were involved in rear-end collisions. The residual symptoms at follow-up were tabulated (Table 20.1) with neck pain the most common symptom, followed by paraesthesia. Auditory symptoms comprised tinnitus and deafness in equal proportion.

Patients were grouped according to symptom severity: group A (12%) considered they were completely recovered. Group B (48%) had mild symptoms which did not interfere with work or leisure. Group C (28%) complained of intrusive symptoms which necessitated analgesics, orthoses or physiotherapy. Group D (12%) suffered severe problems, had lost their jobs and relied continually on orthoses or analgesics and had undergone repeated medical consultations. Other such studies are quoted in this section. My point in bringing this forward is that I have no reason to think that in most cases were soft tissues of these people handled in any way. This is a book about "Manual Therapy of the Vertebral Column" after all; its whole raison d'etre is to zoom in and justify bone waggling, or handling of the hardest mesoderm of the body. Handling the bones means ignoring the soft tissue that gets squished between the bones and the practitioners hand, including skin, including all the responses the nervous system is trying desperately to signal through its organization of soft tissue behavior.

PT practice patterns work against soft tissues being handled in most cases even today, let alone any way that respects or is informed by information currently available about the nervous system. How are practitioners going to be developed who can learn to do this, given the lack of research fascination with it, and the 4-6 patients/per hour case load scenario? To leave soft tissues and skin out of the treatment picture is simply bad practice, in that they are self regulating if given a chance, in that most of the PNS is within them, and given that right handling would go a long way to prevent their becoming ongoing "nocioceptive drivers." I could go on about this for hours, but I will spare you.

[Jon Newman]

I'm going to try not to bog down the "five questions" thread with info regarding the ANS but the conversation there inspired me to further reduce my ignorance in this area. I dug out our neuroscience text from PT school (co-authored by Eric Kandel, you may have heard of him).

Some basics:

The ANS has three divisions, not two. They consist of the well known parasympathetic and sympathetic systems. However, it also has an enteric division. All three differ in anatomy and organization. Apparently the enteric system can function autonomously but CNS reflexes are usually directing the show. "The enteric system is regulated by an extrinsic innervation that is supplied by the parasympathetic and sympathetic systems....The innervation of the gut by the sympathetic and parasympathetic fibers of the autonomic nervous system provides a second level of control of motility and secretion, but also can override intrinsic enteric activity in situations of emergency or stress."

But back to temperature (from the five questions thread):

"In the system of temperature regulation, the integrator and many controlling elements appear to be located in the hypothalamus....The feedback detector appears to collect information about body temperature from two main sources: peripheral temperature receptors located throughout the body (in the skin, spinal cord, and viscera) and central temperature receptors concentrated in the hypothalamus...The hypothalamic receptors are probably neurons whose firing rate is highly dependent on local temperature, which in turn is determined primarily by the temperature of the blood."

[Diane]

Yay! Basics are good! :)
Thanks for that. I think we should copy that portion of the 5 questions discussion to this thread.

[Jon Newman]

From Prinicples of neural science (3rd ed.), Kandel, Schwartz and Jessell:

Recordings from neurons in the preoptic area and anterior hypothalamus by Tetsuro Hori, Jack Boulant, and their colleagues support the idea that the hypothalamus integrates peripheral and central information relevant to temperature regulation. Units in this region, called warm-sensitive neurons, increase their firing when the local hypothalamic tissue is warmed. Other neurons, called cold-sensitive neurons, respond to local cooling. The warm-sensitive neurons, in addition to responding to local brain warming, are generally excited by warming of the skin or spinal cord and are inhibited by cooling of the skin or spinal cord. The cold-sensitive neurons exhibit the opposite behavior. Thus, these neurons could serve to integrate thermal information from the periphery with that from the brain. Furthermore, many temperature-sensitive neurons also respond to nonthermal stimuli, such as osmolarity, glucose, sex steroids and blood pressure.

[Diane]

This next section of Grieve's article shows some photos of huge spine osteophytes presumed to be sticking forward into the sympathetic chain. 3. Musculoskeletal changes: lesions of trespass
The involvement of preganglionic sympathetic neurons, in lesions of neural trespass or radiculitis in the neighbourhood of intervertebral foramina T1-L2, is virtually inevitable, with consequences which are well understood.

So far as the thoracic spine is concerned, a fairly detailed review of benign and malignant forms of trespass is given in Chapter 29 together with some forms of neuropathy.

Sympathetic neurons may be compromised in other ways, for example (a) by osteophytes (spondylophytes) of intervertebral bodies on the anterior and anterolateral aspects of thoracic and lumbar regions, (b) by arthrotic changes of costovertebral articulations (Nathan 1984) - in the thorax the sympathetic chain lies on the heads of ribs, (c) acquired and/or congenital spinal stenosis (Grieve 1988). Chronic compression of the cauda equina produces not only the vascular features of intermittant claudication but also severe bilateral leg pain, (d) Nathan et al (1982) describe an osseous-fibrous tunnel on the ala of the sacrum, and the considerable variations in size and strength of the lumbosacral ligament which helps to form it. This structure may be a factor in L5 root compression, which can include a sympathetic ramus communicans.

The greater and/or lesser splanchnic nerves, more especially on the right side in the thoracic spine, are often stretched over bony excresences and sometimes incorporated in fibrotic thickenings of connective tissue. They are similar to those in the lumbar spine.

Nathan's (1969) dissections of 344 cadavers revealed predominantly right-sided thoracic osteophytes trespass involving splanchnic nerves in 60.7% of the cases studied.

Nathan (1968) also dissected 390 lumbar sympathetic trunks from 195 adult cadavers. Osteophytes (spondylophytes) were found compressing the sympathetic trunks to some degree in 153 (78.4%) of the cadavers.

The macroscopic changes produced by osteophytic compression were enlargement, angulation and colour changes of the ganglioa, accompanied at times by a sclerotic reaction and adhesion to the surrounding tissue.

The highest incidence was at the L4-L5 interverebral joint, rather more frequently on the right side. The author speculates that symptoms of compression may be expected to appear in the lower limbs and/or pelvic viscera, since features of sympathetic dysfunction are not uncommon in adults and elderly people.

Stewart (1931) described a case of intermittent claudication, in which all the clinical features of early thorombo angiitis obliterans were evident, although radiography did not reveal any arterial sclerotic change. At operation on the left lumbar sympathetic chain, extensive degenerative hypertrophy was revealed extending from L3 to L5. Between L4 and L5 the sympathetic trunk was embedded in a mass of hypertrophic tissue, and was dissected free with great difficulty. Compared with the trunk above this level, the freed section appeared to be contracted. Postoperatively, the left leg was distinctly pinker and warmer than the unoperated right leg.

So. My mind immediately jumps to.. 1. this is horrible, and; 2. how can we try to prevent this happening?
In a seated position, psoas is active. It is attached to the fronts of the vertebral bodies and exerts a pull on them. Could that be helping form osteophytes.. Woolf's law? (Woolfe's law: "Bone accommodates the forces applied to it by altering its amount and distribution of mass.")
So, I'm thinking, less sitting, more prone extension to 1. elongate front of the spine neural tissue (preventively), and; 2. keep the contractile (voluntary or involuntary) stuctures in front of the spine eccentrically lengthenable; (c) maintain slidiness of the lumbar sacral plexuses through the psoases; (d) hopefully keep these big nasty things from growing in the first place and keep the circulatory function to the legs optimal.

Next, section 4. Autonomic nerve involvement in referred pain and other symptoms.

[Diane]

Last section in this chapter.
4. Autonomic nerve involvement in referred pain and other symptoms

Most, if not all, peripheral branches from spinal nerves contain postganglionic sympathetic fibres (Williams et al 1989).

Bourdillon and Day (1987) suggested that the precise role of autonomic nerves in appreciation of pain remains to be clarified; so also do the precise pathways and peripheral destinations of postganglionic sympathetic neurons.

For example Keele and Neil (1971) and others, tabulated the sympathetic supply to the head and neck as follows;
Eye: T1,2; superior cervical, along internal carotid artery
Face: T1,2; superior cervical, along external carotid artery
Skin of head and neck: T1,2; superior cervical, with cervical plexus
Cerebral vessels T1, 2; superior and inferior cervical, along internal carotid and vertebral arteries.

The lowest somatic segmental supply to the upper limb is T3, while the sympathetic supply to the upper limb may be derived as far caudally as T8.

There is experimental evidence in man that pain afferents from the face pass back to upper thoracic segments and thus the spinal cord via the cervical sympathetic chain, i.e., in addition to the multitude of cranial nerve afferent neurons which descend in the spinal tract of the fifth cranial nerve before synapsing in the dorsal region of C1, C2, and C3 segments, as do the somatic afferents of those segments.

Electrical stimulation of the superior cervical sympathetic ganglion can produce pain in the face - precisely the same result is produced when the cervical sympathetic trunk is sectioned and the proximal ends are again stimulated (Smith 1969).

Pain is often referred from spinal segments to body parts which have no nerve connections other than via autonomic nerves. Unnecessary difficulty can arise because of restricted concepts about the cause of clinical features. Referred pain in the head, neck, trunk, and limbs may be thought about in stereotyped ways which might be briefly tabulated as in table 20.3.

Head and neck: Intracranial and extracranial head lesions; temporomandibular joint; upper cervical segments
Upper limb: Lower cervical and uppermost thoracic segments; some diseases of thoracic viscera
Trunk wall: Thoracic and uppermost lumbar segments; some diseases of thoracic and abdominal viscera
Lower limb: Mid/lower lumbar segments; pelvic articulations and hip-joint

We tend to concieve musculoskeletal referred pain in neck, trunk and limb to be a matter of somatic neurons alone, yet readily accept the phenomenon of visceral lesions referring cutaneous pain and tenderness to trunk areas and, in cardiac disease, the left upper limb. Where somatic nerve connections do not exist, e.g. (a) between mid-thoracic segments T345 and the head, and (b) between thoracic segments T4 and caudally and the upper limbs (Ch 29), clinical familiarity and acceptance of pain referred (if that is the right word) in these ways is remarkably thin on the ground, despite the regularity with which manual therapists relieve head pain, and bilateral glove parasthesiae of upper limbs, for example, by simple mobilization of the named thoracic segments.

Our understanding of referred pain is incomplete. Sufficient clinical experience exists to suggest that autonomic nerves may share more actively in the mechanisms underlying its vagaries.

Although much remains to be learnt of the afferent routes of impulses arising in painful pathological conditions of viscera (Willams et al 1989), visceral afferents from the heart are manifestly capable, in cardiac disease, of initiating referred pain down the left arm. Why should this known propensity not be acceptable as a central mechanism in referred musculoskeletal pain too? There are no known visceral aferents from skeletal tissues, but might not the cortical representations of skeletal tissues include the autonomic innervation of blood vessels? Why should not the rich autonomic innervation, and thus cortical representation, have as much to do with patterns of referred somatic pain as somatic nerve representation? This may well explain the notorious untidiness of referred pains, which do not respect (somatic) dermotomes. The question has not yet, to my knowledge, been fully addressed by the many writers on referred musculoskeletal pain.

From Grieve's Conclusion section:
- (re: capasular, ligamentous and tendinous lesions..)"Much is made of friction massage, mobilization, stretching, manipulation, ultrasound, acupuncture, hydrocortisone, cock-up supports, and so on, yet the condition remains notoriously treatment-resistant and the passage of time is usually the one factor which helps many to recover.
- "Bryan et al (1990) investigated peripheral sensory function in reflex sympathetic dystrophy, noting a significant elevation of skin temperature, and a lowering of the pressure pain threshold, in the affected limb. They hypothesize that this leads to further changes in autonomic tone, thus establishing a pathological loop of activity. Sympathetic block abolished pain by allowing peripheral receptors to revert to normal thresholds in the 40 patients of their study. That sympathetic nerve distribution may be an important factor in patterns of referred pain, of musculoskeletal origin, should perhaps be more widely recognized as should the phenomenon of secondary pathology of the soft tissues in areas to which pain is commonly referred from primary axial lesions." (Well, if your belief system is based entirely upon the idea of primary axial lesions, Gregory..:rolleyes: ..otherwise I would concur..)

I plan to bring Butler's POV (from SNS) to this thread, anatomical tidbits from Grey's, and bits of Burnstock.

[Diane]

Ian's link (http://www.in-cites.com/papers/MichaelCaterina.html). This is an interview with Dr. Michael Caterina who talks about his work on 'chili pepper extract' in Nature in 1997, and where it is taking him.
“What we reasoned was that no one had ever identified capsaicin inside the body, so it seemed unlikely that nature had put this channel in our pain-sensing neurons just so we could enjoy eating spicy foods.”

[Diane]

Here is a good sample of Butler's clarity on the matter at hand. From P 84-92:
IMMUNE, ENDOCRINE, MOTOR AND SYMPATHETIC SYSTEMS AS RESPONSE AND BACKGROUND SYSTEMS
INTRODUCTION
The nervous system processes and gives value to any input. Sometimes this value judgement is visibly expressed via the sympathetic (e.g., sweating, redness) or the motor system (spasm, withdrawal, learnt movement patterns). The responses of other systems such as the immune and endocrine systems remain hidden, at least initially, but could be measured. Nervous system response computations are extremely complex, individual and situation specific. They are usually survival driven but often disturbed by novel modern psychosocial demands.

The systems involved often work synergistically. Although considered as response systems, these systems are also closely associated background homeostatic systems, operating at the same time as signalling in the peripheral and central nervous systems.

Systems such as the endocrine, immune and autonomic are foremost protective systems, yet while they can protect and heal, something which requires considerable power, they can also damage, especially in states of maintained stress and pain. Clinical patterns from the activities of these systems are not as obvious as say, peripheral neurogenic pain. Thee is much synergystic activity betweeen systems, and like all pathobiological mechanisms they will always be in action. In extreme states, the systems will become evident, for example the motor system in focal dystonia, the sympathetic nervous system in complex regional pain syndrome and the endocrine and immune system in Cushing's disease and rheumatoid arthritis. Chronic pain probably involves maladaptive responses in all systems.

A useful way to link things together is to look at the integrated actions of the stress response, remembering that pain is probably the ultimate stressor. Stress biology has only recently been associated with the neurobiology of pain (e.g., Gifford 1998; Melzack 1999; Melzack 1999). Such links and use of the clinical consequences are long overdue. Useful general references include Fink (2000), Sapolsky (1994), Lovallo (1997), and Martin (1997).

AUTONOMIC/NEUROENDOCRINE SYSTEM
Pain and stress will activate three key circuits - the hypothalamus-pituitary-adrenal axis (HPA), the sympathoadrenal axis (SA) and the sympathetic neural axis. These are the peripheral limbs of the stress system. The central components are located in the brainstem and hypothalamus. These axes are linked to other brain areas with interests in survival such as the amygdala, multiple cortical areas and the motor system. These three circuits will respond to a variety of signalling including blood borne, sensory, limbic and circadian signals. The circuits will also respond to immune mediated inflammatory moloecules such as tumour necrosis factor alpha and the interleukins 1 and 6.

Pain nearly always acts as a stressor. The activities of these stress systems will also be integrated into the overall CNS processing of pain.

THE HYPOTHALAMUS-PITUITARY-ADRENAL AXIS
Paired adrenal glands, perched on top of the kidneys and essential for life are two of the key structures (Fig. 4.5). They have a central medulla and outer cortex. Both areas function in times of stress, but secrete different chemicals; adrenaline and noradrenaline from the medulla (sympathoadrenal axis) and corticosteroids (cortisol) from the cortex. The cortex is part of the HPA axis.

Cortisol secretions are activated by the adrenocorticotrophic hormone (ACTH) secreted into the blood from the anterior pituitary gland. ACTH secretions, matched by cortisol secretions are high in the morning, low in the evening but stimulated by all forms of stress over 24 hours. Forms of stress such as pain, injury, thoughts, feelings, deeds of others, memories and environmental changes are signalled via corticotrophin releasing hormone (CRH) from the hypothalamus to the pituitary gland (Fig 4.5). The actions of CRH are inhibited by blood cortisol levels which are sampled by the hypothalamus. A feedback system is therefore in operation. CRH neurones and noradrenergic neurones innervate and stimulate each other in the brain, thus linking the stress systems (Chrousos 1995).

CORTISOL
It is the adrenal cortex and its secretion cortisol which are particularly critical to life. Almost all tissues of the body have receptors for cortisol, including the brain. Cortisol gets a bad rap as a stress chemical, but it is vital to life. It maintains cardiovascular and metabolic homeostasis, in particular stimulating protein catabolism and glycogen synthesis - vital energy for dealing with emergencies. In addition, cortisol can cross the blood brain barrier and effect brain structures, one result being mood changes including depression. Cortisol can also exert regulatory effects on the inflammatory and immune responses through the inhibition of cytokine action and production. For reviews, see Lovallo (1997), Fink (2000), and Sternberg and Gold (1997).

In an emergency, cortisol shuts down activities not needed for survival and enhances those that are. Hence the inflammatory and immune systems, digestive and reproductive systems are shut down. With the proverbial tiger confrontation, reproduction, digestion, and wound healing are not high priorites - they can wait for later. Energy goes to systems which can help avoid the stress and contribute to survival, such as the cardiovascular system, brain, and muscles, i.e. be smart, think clearly, and perhaps run very fast.

A chronic excess of cortisol as in chronic pain or stress poses problems. Cushing's syndrome (chronic hypercortisolism) is an extremem example. The features include immunosuppression, osteoporosis, cardiovascular disease, depression and insulin resistance (Whitehouse 2000). More subtle cases of tissue degeneration, mood swings, slow tissue healing and susceptability to infection may be noted by clinicians managing patients with chronic pain.

SYMPATHETIC NEURAL AXIS AND SYMPATHETIC ADRENAL AXIS
The HPA axis is closely linked to the sympathetic nervous system (SNS) by links from the hypothalamus to the locus ceruleus, a key sympathetic nervous system control network in the brainstem. The SNS is also mobilized in times of stress, it innervates immune organs as well as nearly every tissue in the body. Stimulation will evoke arousal, fear, and readiness.

The SNS also plays a role in the stress response and body homeostatic function. A well known figure demonstrating the sympathetic nervous system is in figure 4.6. Note that this one is slightly different from most in that it aknowledges that muscles, joints, skin and the connective tissue sheaths of the nervous system have a sympathetic innervation. The sympathetic nervous system output to the entire body iemerges from slinal levels T1 to L3. The paired trunks are continuous, connective tissue sheathed preganglionic structures, and are known to evoke pain if stimulated (Walker and Nulson 1948; Echlin 1949). One preganglionic sympathetic neurone will diverge onto 15 or more postganglionic neurones (Wolf 1941). Its physical health may be of interest to manual therapists (chapter 15). This part of the nervous system is very glandular - noradrenaline can dribble out of numerous varicosities along postganglionic fibres (Chapter 3).

Altough sympathetic responses are ususally widespread (e.g. total limb or body sweating), the sympathetic nervous system has varying layers of control from local organ to the brain (Lovallo and Sollers 2000). Local organ control allows, for example, blood flow adjustments to muscles, another control layer is ganglionic mechanisms which regulate the output of the postganglionic neurones and then the brain and hypothalamus regulate the entire system. The first two respond more to physiological challenges, the brain responds more to psychological stress.

The sympathoadrenal axis is a powerful part of the sympathetic nervous system. Note in figure 4.6 that the adrenal medulla receives a direct sympathetic preganglionic innervation from the spinal cord. This allows secretion of adrenaline and a little noradrenaline directly and rapidly into the bloodstream. This is known as the sympathetic adrenal axis.

ADRENALIN/NORADRENALINE
Mental and physical effects and psychosocial conditions evoke adrenaline and noradrenaline secretions. Mental stress causes more adrenaline secretion whereas physical stress, linked with more physical activity and blood pressure homeostasis evokes more noradrenaline (Lundberg 2000).

Both adrenaline and noradrenaline prepare us for action. They stimulate cardiovascular responses, blood is shunted to the heart, muscles and brain and away from the digestive system and skin. They promote increased levels of glucose and free fatty acids. More oxygen is available, sweating occurs to cool the body and make it slippery. Via its immune organ innervation, these catacholamines can modulate inflammation. Adrealine is immunosuppressive by altering lymphocyte production from the spleen. These are useful secretions for an emergency, but like cortisol, maintained high levels lead to the risk of cardiovascular disease and tissue damage.

Normal or threshold levels of adrenaline do not exist. Levels may double during mild stress such as daily work. Severe stress with emotional demands may cause levels to rise 10 times the resting level for that person. Novel inputs and anticipation markedly raise adrenaline levels (Lunfberg 2000). However an increased level of adrenaline does not necessarily mean pain. While the levels surely contribute, an upregulated sensory system involving inflammation and adrenoreceptors will be necessary for adrenaline and noradrenaline to access the pain system.

SYMPATHETIC NERVOUS SYSTEM AND PAIN
The sympathetic nervous system can contribute to the sensitivity of inflamed tissues and it can also contribute to the sensitivity of damaged nerves. This can be seen spectacularly with increases in pain if adrenaline is injected into patients with nerve injuries such as a neuroma (Chabal et al 1992; Raja et al 1998). However, adrenaline injected into a person with no nerve injury will be painless.

The sympathetic nervous system is essentially a motor system. To cause pain it must somehow activate the afferent system, especially C and A-delta fibres if the CNS is sensitized. Understanding this pain comes back to receptors. Adrenaline itself does not hurt, it needs receptors attached to nocioceptors to contribute to pain or it must contribute to a chemical soup which activates nocioceptors. Therare thus three places where adrenaline may activate the afferent system. These are contributions to inflammatory soup, contributions to and AIGS or influences due to adrenoreceptor upregulation at the DRG. Adrenaline can act as a central excitatory neurotransmitter, thus it may contribute to the magnification of afferent input. There are more details in chapter 3. Review also figure 3.9.

The stress chemicals such as noradrenaline and cortisol could also contribute to input via destructive effects on tissues. Persistent high level bathing by cortisol and catecholamines appears to have a deleterious effect on connective tissues (Oxlund and Manthorpe 1982; Curwin et al. 1988; Eyre 1990). Noradrenaline pathways in the brain are also closely linked to negative emotional states.

THE PARASYMPATHETIC NERVOUS SYSTEM
Often forgotten with the excitement of the sympathetic nervous system is the parasympathetic nervous system. "Flight and fight" has reminded generations of students about the role of the sympathetic nervous system. The catch cry of the parasympathetic nervous system - "rest and digest" was also proposed by Cannon (Kandel et al 1995), and is just as important for students and patients to understand. Usually these two systems balance each other. The parasympathetic nervous system is more operational at rest when it repairs and heals the tissue traumas of the day.

It may be worthwhile telling patients about this healing and helping system, particularly when talking about sleep health and the need for some patients to introduce relaxation as a coping strategy. To be continued. Next, MOTOR SYSTEM AS AN OUTPUT SYSTEM.

I would beg to quibble slightly with Butler about the effects of sympathetic shunting in the brain. He says blood flow is increased to the brain. I would want to ask, which parts? My contention is that blood flow likely increases to the parts that decode vision, equilibrium, motor planning, rage etc.. all the non-conscious mechanisms for enhancing escape. I seriously doubt this involves any sort of thinking in the usual sense of the word, in other words, if a tiger is going to bite you, you aren't going to bother to put a finger to your head to ponder in that moment if it is a Siberian tiger or a Sumatran tiger, or work out the evolutionary tree and where they might have diverged, or stop to chat to your child about the difference in a moment of verbal social grooming. Not really. Chances are the danger would strike one mute except for perhaps a howl issuing from some preverbal part of the more non-conscious brain. So my understanding is that blood flow or at least glucose uptake is actually decreased to the frontals in lots of places and increased elsewhere. Aftrer all, the brain is not monolithic, and lots of the planning/escape centres are evolutionarily much older than the "human" bits.

[Diane]

MOTOR SYSTEM AS AN OUTPUT SYSTEM
Muscles can be inflamed, acidic and weak and hence be potent sites of high threshold input into the CNS. There are secondary effects of damaged muscle also, for example joint instability or a change of the container tissue around a peripheral nerve, all of which could contribute to primary or secondary hyperalgesia.

The motor system can also be conceptualized as a response system. Motor responses to pain and stress include weakness, spasm, changes in facial expressions and tone of voice, muscle imbalances, loss of quality and range of movement, loss of variety of movement selections etc. To some degree these changes are a product of the physical health of the muscles, but they are also products of central processing and are essentially coping mechanisms. Like the increased cortisol in acute stress, some spasm and muscle tension (e.g., Knost et al 1999), even a change in tone of voice are useful in acute pain and injury if it enables optimal management. If they persist then these once useful behaviors become maladaptive and destructive to outcome.

A hyperactive sensory system will have repercussions for the motor system (Woolf 1984) as well as the other output systems. Like the sympathetic nervous system, there are local responses such as spasm and ill-health of collagen. There are also observable changes in patterns of gross movement and postures as people cope. These are often conceptualized as muscle imbalance syndromes. The decreased movement options available and the learned habits of the chronic pain sufferer may lead to deconditioning.

Muscles will react to thoughts. The cortical activity which occurs at the thought of a movement is similar to the cortical activity when the movement occurs (Lotze et al 1999). In an experimental situation patients with chronic low back pain who discussed pain episodes had elevated EMG activity compared to those exposed to neutral stimuli (Flor et al 1992). Powerful psychophysiological influences on motor behavior include fear of movement, fear of reinjury, and fear of pain (for recent reviews see Vlaeyen et al 1995; Crombez et al 1999; Vlaeyen and Crombez 1999).

The straight leg raise (SLR) is one of the key neurodynamic tests (Chapter 11). McCracken et al. (1993) showed that anxiety related to pain was a predictor of pain level and range of SLR movement in chronic low back pain patients.

IMMUNE SYSTEM
BASIC APPARATUS
The days of considering the immune system as a separate system to the nervous system are gone and there are now well defined multilevel and reciprocal links between the immune system and the nervous system. For reviews of the nervous system and pain see Watkins (2000), Watkins and Maier (1999), Black (1995) and Sternberg and Gold (1997).

The immune system comprises organs (bone marrow, thymus, lymph nodes, and spleen) and various cells (T cells, B cells, natural killer cells, macrophages, and neutrophils). It also comprises messenger molecules known as the cytokines, which allow communication between cells. Sternberg and Gold (1997) note that the immune and nervous systems are quite similar in that they possess sensory elements which recieve information from the body and the environment, and they possess motor elements to carry out responses. The cytokines fulfil that role and are of particular interest here.

CYTOKINES
Cytokines are produced in response to various physical and emotional stressors. They have a critical role in infection control and can powerfully contribute to inflammation and pain. Some cytokines are anti-inflammatory and some are pro-inflammatory, making something of a balance. The identified pro-inflammatory cytokines are interleukin-1 (IL-1), interleukin-2 (IL-2), and Tumour Necrosis Factor Alpha (TNF alpha), called TNF alpha because it will cause a haemorrhaging necrosis of tumours if injected into animals. It's apparently powerful stuff. The anti-inflammatory ones include IL-4, IL-10 and IL-13. If a human is injected with IL-1, fever, headache, joint and muscle pain will ensue (Dinarello 1999). IL-1 also stimulates prostaglandin and phospholipase A2 synthesis as part of a contribution to the chemical cascade of inflammation. For reviews see Marshall (2000) and Watkins (1999).
The immune system is powerfully regulated by the peripheral and central nervous systems, although this signalling is not all one way. Any CNS activation via physical and psychological stressors may result in immunity changes (Ligier and Sternberg 2000). Activation of the HPA axis and the sympathetic nervous system axes will effect immunity primarily by release of cortisol. See figure 4.7. The sympathetic nervous system also modulates the immune system through its innervation of the immune organs such as the spleen and lymph nodes. Peripheral nerve responses such as substance P (Dickerson et al. 1998) will activate pro-inflammatory cytokines.

The proinflammatory cytokines IL-1, IL-2 and TNF alpha can also signal the nervous system in a number of ways. Cytokine signalling can occur through its stimulatory effects on the inflammatory soup and in damaged peripheral nerve as discussed in chapter 3. Cytokines have an influence in the brain also, but these large proteins have some difficulty crossing the bloood-brain barrier. They require a leaky section to pass. Another mode of signalling is thought to involve sensory paraganglia attached to the vagus nerve (Maier et al 1998; Watkins and Maier 2000). The vagus nerve terinates in the nucleus tractius solitarius which has links to many areas such as the hippocampus and hypothalamus. Glia in the spinal cord and brain will respond to immune signalling by synthesizing and releasing IL-1 and thus stimulating the release of further neuroactive substances such as nitric oxide, NGF and excitatory amino acids such as glutamate. Interleukin 1 can potentiate secretion of corticotrophin releasing factor and thus a stress response. (Watkins et al. 1994; Watkins and Maier 2000). The brain is perghaps the most prolific endocrine organ in the body (Sternberg and Gold 1997).

THOUGHTS FOR CLINICIANS
Much is made of our stress response systems having to function in the age of computers, bureaucracy, new diseases, pollution and job stress, all with a design based on the needs of many thousands of years ago. As Nesse and Young (2000) suggest, we may have forgotten that the ancestral physical stresses of no police, no food resources, no laws, rampant diseases and predators were/are also extremely powerful.

The majority of research articles about pain mechanisms state that their hope is that the findings may lead to improved pharmacological inteventions. Only a few look at other options and realize that the non-drug management potential is also increasing and the side effects may be less. In addition to improving tissue health, cardiovascular fitness and applying various movement enhancement strategies, there are a number of psychosocial variables which can be manipulated by movement based therapists as a management strategy or to enhance a physical strategy. For example, optimism, motivation, coping methods, an understanding of the meaning of pain, and social support will all, to some degree, protect against the psychological, cardiovascular, endocrine, and immune effects of stress. The reasoning models proposed in chapters 6 and 7 should allow integration of all pain mechanisms. In figure 4.8, there is a summary of the pain mechanisms. This links the peripheral mechanisms (chapter 3) with the central and response mechanisms in this chapter. The part about vagus, usually thought of as a parasymathetic nervous system structure, being part of the immune system function is interesting. See attached thumbnails. The flow chart with rectangles is great. But I have wandered away from the autonomics as such. I'll wander back in again.. topical issues in pain, Gray's, etc.

[nari]

These might be helpful - the study that demonstrated the vagus's role in the immune system.
http://www.northshorelij.com/body.cfm?id=204&action=detail&ref=616

http://nature.com/nature/journal/v241/n6921/full/421328a.html

Nari

[Diane]

Thanks Nari. Great!
The link to nature.com only goes to an index of articles, not THE article.. if you have it, could you attach the actual article or send it by email so we could put it in sounds of silence (if it's copyright, which I'm sure is the problem)?

[nari]

That's weird. I typed in the URL of the article - don't know what happened there. Will try again.

Nari

PS I could not work it out, so have just sent the article to you.
It is surprising that Nature allows access to full articles - usually there is none.

[Diane]

http://www.nature.com/nature/journal/v421/n6921/full/421328a.html
Inflammation: A nervous connection

Claude Libert
Top of page
Abstract

The molecular details of a connection between the nervous system and the inflammatory response to disease have been uncovered. This suggests new avenues of research into controlling excessive inflammation.

Sepsis is a complex, exaggerated and chaotic version of the usually well-organized inflammatory arm of our immune defences, and kills over 175,000 people each year in the United States alone1. Although a great deal of time and effort has been spent researching septic shock, it remains difficult to understand and treat. One promising lead was provided two years ago, when it was discovered that there is a connection between inflammation and the involuntary nervous system. The details of this link have, however, been unclear — until now. Writing on page 384 of this issue, Kevin Tracey and colleagues2 describe how they identified a receptor protein that is stimulated by the nervous system and which in turn inhibits a key molecular mediator of inflammation and septic shock. This receptor might make a good target for future drugs to treat sepsis.

Inflammation has several roles in the body, one of which is to contribute to the immune system's ability to fight off intruding microorganisms. For instance, molecules that are produced during the inflammatory response increase blood flow to infected areas, or help to recruit immune cells. One way in which inflammation is triggered is in response to lipopolysaccharides — components of the cell walls of many bacteria — which activate the immune system's macrophages. These cells in turn release 'alarm' molecules, namely cytokines, some of which have powerful pro-inflammatory properties. Tumour-necrosis factor (TNF) is one such molecule. This protein can affect nearly all cell types, and has a range of biological activities. For instance, it induces the expression of a large number of genes that encode essential inflammatory molecules (such as other cytokines; enzymes that help to break down the barriers between cells, allowing the migration of immune cells; and adhesion molecules that again enhance immune-cell migration)3, 4.

As long as TNF production remains confined to the site of infection, the inflammatory response is clearly beneficial. But once bacteria, and consequently TNF, invade the systemic blood circulation, blood 'poisoning' and sepsis can develop quickly. Furthermore, TNF has been found to be a central mediator of chronic inflammatory disorders such as rheumatoid arthritis and Crohn's disease. So there is much interest in learning how to control the production, release and activity of TNF. Several means of doing so have been developed (Fig. 1), and have seen some success in treating certain inflammatory disorders5. For instance, there are drugs that inhibit the transcription of the TNF-encoding gene into messenger RNA, the translation of the mRNA into protein, or the release of the TNF protein. There are also antibodies and soluble receptors that bind to and block TNF once it has been released. But, although the value of these approaches is beyond doubt, they all take time to work — and time is usually short when treating patients with sepsis.
Figure 1: The inflammatory response to microorganisms, and ways of controlling it.
Figure 1 : The inflammatory response to microorganisms, and ways of controlling it. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Clockwise from lower right: many bacteria contain lipopolysaccharide in their cell walls, which stimulates macrophages. These immune cells then make and release various cytokine ('alarm') molecules, including tumour-necrosis factor (TNF) and interleukin-1. But too much TNF in the blood can be harmful, leading to excessive inflammation and septic shock. Several drugs (orange boxes) inhibit steps in TNF synthesis. In addition, Tracey and colleagues have found that when the vagus nerve detects interleukin-1 (left), it releases acetylcholine (right), which binds to the alpha7 receptor2 on macrophages and inhibits cytokine production. This suggests possible new ways of controlling inflammation: through electrically stimulating the vagus nerve, by acupuncture, or with the use of nicotine (which mimics acetylcholine).
High resolution image and legend (45K)

Tracey's research team has been studying TNF since this protein was discovered (see, for instance, ref. 6). Recently, Tracey's group described another level of control of TNF synthesis — namely by means of the vagus nerve7 — thereby providing a new and exciting link between the involuntary nervous system and inflammation. This 'parasympathetic' nerve emanates from the cranium and innervates all major organs in a subconscious way. It is finely branched and is composed of both sensory (input) and motor (output) fibres. This is of relevance because it means that the vagus nerve can on the one hand sense continuing inflammation (presumably by detecting cytokines through receptors on the nerve surface), and on the other hand suppress it. This suppression is efficient and, above all, a good deal faster than the mechanisms mentioned above. Tracey's group found7 that, after injecting lipopolysaccharides into rats, electrically stimulating the vagus nerve prevented both the release of TNF from macrophages, and death. Conversely, surgically severing the nerve not only removed this protection but also sensitized the animals to lipopolysaccharide.

But how does the vagus nerve have this effect on macrophages? It was already known that, after this nerve is stimulated, its endings release the neurotransmitter molecule acetylcholine with lightning speed. Macrophages express acetylcholine receptors known as nicotinic receptors, and respond to the released acetylcholine (or the acetylcholine-mimicking nicotine) by suppressing TNF release. But the precise identity of the nicotinic receptors on macrophages was not known. From a therapeutic point of view, this is clearly important to know. It's also very difficult to find out, as the receptors are pentamers containing different combinations of a possible 16 monomers.

In their latest paper, Tracey and colleagues2 pin down the relevant nicotinic acetylcholine receptor: it is one comprising five copies of the monomer alpha7. They started by using alpha-bungarotoxin, a molecule that binds to just a subset of receptor monomers, to show that macrophages express the alpha7 subunit. When the authors blocked the expression of this protein, acetylcholine and nicotine were no longer able to prevent the release of TNF — data that the authors confirmed by studying alpha7-deficient mice. In fact, such mutant mice displayed an exaggerated response to lipopolysaccharide in terms of their production of the cytokines TNF, interleukin-1 and interleukin-6. Finally, in a technical tour de force, Tracey and colleagues showed that electrically stimulating the vagus nerve of alpha7-deficient mice no longer afforded protection against lipopolysaccharide (in contrast to the situation in wild-type mice).

These findings2 could have therapeutic implications. The discovery of the connection between the involuntary nervous system and inflammation had already yielded new ideas about treating inflammatory disorders such as sepsis: for instance, a small compound has been developed that can trigger the vagus nerve in rats, thereby reducing inflammation8. Looking to the future, it would be interesting to stimulate the vagus nerve electrically in people — as is currently done in thousands of epilepsy patients, showing that the procedure is safe and feasible — and to study the effect on inflammation. More specifically, the new findings suggest that molecules that stimulate the alpha7 subunit would also be worth developing.

On a different note, nicotine has been found to have powerful immunosuppressive and inflammation-suppressing effects. Of course, the health risks associated with smoking are immense. Yet epidemiological studies indicate that nicotine protects against several inflammatory diseases, such as ulcerative colitis, Parkinson's disease and even Alzheimer's disease. It can also reduce fever and protect against otherwise lethal infection with the influenza virus9. The demonstration2 that nicotine binds to the alpha7 subunit on macrophages fleshes out the details of how nicotine produces such effects.

The data also make me reconsider the possibilities and molecular biology of 'alternative' medicine. Pavlovian-type conditioning, hypnosis and meditation are well known (since the beginning of the twentieth century in some cases) to reduce inflammation10. It might be worth finding out whether these effects, as well as the reported beneficial effects of prayer and acupuncture on inflammation (the last of which is known to depend on acetylcholine)11, 12, are mediated by the vagus nerve and the alpha7 subunit.

Thanks Nari!:thumbs_up
Anyone else, please report if the link doesn't work.. it works fine for me now. Thanks.)

[Diane]

Weirdest thing.. the site won't let me go back in to edit my last post. Oh well..
Sepsis is a complex, exaggerated and chaotic version of the usually well-organized inflammatory arm of our immune defences, and kills over 175,000 people each year in the United States alone1. Although a great deal of time and effort has been spent researching septic shock, it remains difficult to understand and treat.

I wonder if this isn't the organism's way of trying to commit suicide? Like apoptosis, only not at a single-cell level, rather at a multicell level.. We being human, of course, we hate to let go.

[emad]

Hope this good link :

http://education.yahoo.com/reference/gray/

Regards
Emad

[Diane]

p. 909: The peripheral nervous system comprises the cranial and spinal nerves and the peripheral part of the autonomic nervous system (see p. 1292) including the enteric nervous system (composed of plexuses of nerve fibres and cell bodies in the wall of the alimentary tract). The peripheral nervous system is composed of the axons of motor neurons situated inside the central nervous system, and the cell bodies and processes of neurons grouped together as ganglia (swellings). Sensory ganglion cells in posterior (dorsal) roots give off both centrally and peripherally directed processes, and do not have synapses on their cell bodies, whilst ganglionic neurons of the autonomic nervous system receive synaptic contacts from various sources. The cell bodies situated in peripheral ganglia are all derived embryonically by migration from the neural crest. (p. 147).

On p 146 is just a reminder of what neural crest is about.
On P. 1292 is the real deal on the ANS. Get ready, there are pages and pages of info here to bring on:
GENERAL ORGANIZATION:
The autonomic nervous system posesses both central and peripheral components, the latter being concerned with the innervation of the viscera, glands, blood vessels and non-striated (smooth) muscle. It therefore forms the visceral (splanchnic) component of the nervous system. The term 'autonomic' is a convenient rather than appropriate title. The autonomy of this part of the nervous system is illusory, since it is intimately responsive to changes in somatic activities. While its connections with somatic elements are not always structurally clear, the functional evidence for visceral reflexes stimulated by somatic events are abundant. (For general information consult Langley 1921, Kuntz 1953; Mitchell 1953, 1956; Pick 1970; Gabella 1976; Bjorkland et al 1988; Bannister & Mathias 1992; Burnstock 1992-95.)

Visceral efferent paths differ from their somatic equivalents in being interrupted by peripheral synapses, at least two neurons being interposed between the central nervous connections and visceral effectors (8.392). The somata of the primary neurons are in the visceral efferent nuclei of cranial nerves and in the spinal lateral grey columns; their axons, variably but usually finely myelinated, traverse the cranial and spinal nerves to the peripheral ganglia, where they synapse with the dendrites of somata of secondary neurons. Axons of secondary, effector neurons are usually non-myelinated and supply non-striated muscle or glandular cells. These nerve fibres are also found close to adipocytes, mast cells, melanophores, interstitial cells, autonomic ganglia and motor end plates. There are therefore in peripheral efferent pathways preganglionic and postganglionic neurons, the latter being more numerous; one preganglionic neuron may synapse with 15-20 postganglionic neurons, permitting the wide diffusion of many autonomic effects. This disproportion between preganglionic and postganglionic neurons is said to be greater in the sympathetic than in parasympathetic parts of the autonomic nervous system. (In an investigation into human superior cervical ganglia, a ratio of preganglionic to postganglionic fibres of 1 to 196 was claimed; Ebbesson 1968.) Terminations of postganglionic neurons are described on page 959 and below. For the structure of sympathetic ganglia and details of other neuronal types, including interneurons, see page 1298 et seq.

Visceral afferent paths resemble somatic afferent paths; the cells of origin of their peripheral fibres are unipolar neurons in cranial and dorsal root ganglia. Peripheral processes are distributed through autonomic ganglia or plexuses, or possibly through somatic nerves, without interruption. Their central processes (axons) accompany the somatic afferent fibres through dorsal spinal roots to the CNS (P. 1298).

The autonomic nervous system can be divided into three major parts, parasympathetic, sympathetic, and enteric, which differ in structure and function. The broad anatomical organization of these subdivisions was summarized by Langley in 1921 and has been more or less retained since that time. Parasympathetic preganglionic efferent fibres emerge through certain cranial and sacral spinal nerves as a craniosacral outflow, while sympathetic preganglionic efferent fibres emerge through thoracic and upper lumbar spinal nerves as a thoracolumbar outflow. The somata of parasympathetic postganglionic neurons are peripheral, sited distant from the CNS either in discrete ganglia near to the structures innervated or often dispersed in the walls of the viscera. The somata of sympathetic postganglionic neurons are located mostly in ganglia of the sympathetic trunk or ganglia in more peripheral plexuses but they are almost always nearer to the spinal cord than to the effectors innervated, an exception being some of those innervating pelvic viscera. The enteric nervous system is comprised of ganglionated plexuses localized in the wall of the gastrointestinal tract (p 1749). It contains reflex pathways through which the contractions of the muscular coats of the alimebtary tract, the secretion of gastric acid, intestinal transport of water and electrolytes, mucosal blood flow and other functions are controlled. There are complex interactions between the enteric nervous system and extrinsic parasympathetic, sympathetic and sensory-motor nerves.
The figure 8.392 is a version of the common one of the side view of the spine and all the levels of ganglia with outflow to the organs, eye, etc.etc.
Next, mechanism of transmission. So much juicy stuff in this section.

[Diane]

P. 1294 Gray's: MECHANISM OF TRANSMISSION
It has been considered in the past that physiologically the parasympathetic and sympathetic systems differed in that parasympathetic reactions are generally localized, whereas sympathetic reactions are mass responses. However, even though widespread activation of the sympathetic nervous system may occur, for example in association with fear or rage, it is now recognized that the sympathetic nervous system is also capable of discrete activation, and many different patterns of activation of sympathetic nerves throughout the body occur in response to a wide variety of stimuli.

Parasympathetic activity results in cardiac slowing and an increase in intestinal glandular and peristaltic activities, which may be considered to conserve body energy stores. Sympathetic activity results, for example, in the general constriction of cutaneous arteries (increasing blood supply to the heart, muscles and brain), cardiac acceleration, increase in blood pressure, contraction of sphincters and depression of peristalsis, all of which mobilize body energy stores for dealing with increased activity (MacDonald 1992). I see Gray's uses the term "brain" in general. Hmmnn.
This paragraph sums up the sym/parasym behavior contrast in a nutshell however; skin is drained while the muscle system is fed, when sympathetics are engaged/needed.

For many years the idea of antagonistic, parasympathetic cholenergic and sympathetic adrenergic control of most organs in visceral and cardiovascular systems formed the working basis of all studies. However, major advances have been made since the early 1960s that make it necessary to revise this concept of the mechanism of autonomic transmission. These advances include:(I'm writing out a short list of bullets that isn't in the book, outside the quote box. See further down for detailed list quoted as written):

NANC nerves
Cotransmission
Neuromodulation
Sensory-motor nerves
Intrinsic circuitry
Autonomic neuromuscular junction
Plasticity

NANC nerves. The discovery of non-adrenergic, non-cholinergic (NANC) nerves and the recognition of a multiplicity of neurotransmitter substances in autonomic nerves. Adenosine 5'-triphosphate (ATP) satisfied the criteria as a neurotransmitter in many of these NANC nerves and they were termed 'purinergic' (Burnstock 1972). Subsequently, it became clear that many other neuroactive substances, including many peptides, were present in autonomic nerves. Nitric oxide (NO) or a NO-related compound has recently been showqn to play an important role as a primary messenger in transmitting information from nerves to smooth muscles in specific tissues (Bredt et al 1990; Rand 1992). The list of proposed neurotransmitters and neuromodulators in the autonomic nervous system thus includes monamines, purines, amino acids, a variety of peptides, and NO (P. 935 and Table8.1; Burnstock 1986).

Co-transmission. The concept of cotransmission that proposes that most, if not all, nerves release more than one transmitter (Burnstock 1976, 1990; Hokfelt et al 1986; Kupfermann 1991) and the 'chemical coding' of these nerves to establish the combinations of neurotransmitters contained in individual neurons whose projection and central connections are known. The principal neurotransmitters in most sympathetic nerves are ATP and neuropeptide Y (NPY), although NPY often acts as a neuromodulator. In parasympathetic nerves the principal cotransmitters are actetycholine (ACh), and VIP, with subpopulations utilizing ATP and/or NO. In most sensory-motor nerves (P 968), the neurotransmitters are substance P (SP) and calcitonin gene-related peptide (CGRP), with some utilizing ATP. Other neurotransmitters/neuromodulators are also sometimes colocalized with the principal transmitters in autonomic nerves (8.393). Although there are many different transmitter substances in the gut, most are involved in neurotransmission or neuromodulation at the ganglion level or may be trophic factors. The number involved in neuromuscular transmission is more limited. Enteric NANC inhibitory nerves utilize, probably as cotransmitters, ATP, VIP, and NO whereas enteric excitatory nerves utilize ACh and SP. I'll bring a thumbnail of this diagram. It shows the breakdown of what transmitters are found with which type of nerve.

Neuromodulation. The concept of neuromodulation, where locally released agents can alter neurotransmission either by prejunctional modulation of the amount of transmitter released or by postjunctional modulation of the time course or intensity of action of the transmitter. The wide and variable cleft characteristic of autonomic neuroeffector junctions makes them particularly amenable to the mechanisms of neural control mentioned above. There are many different ways in which cotransmitters and neuromodulators interact to effect neurotransmission including:

- Autoinhibition, by which a transmitter, in addition to its postjunctional effects, modifies its own release, often inhibiting it which may in turn effect the release of cotransmitters;
- Cross-talk, by which a neuromodulator may act on closely juxtaposed terminals;
- Synergism, by which each of two transmitters, either from different nerve terminals or cotransmitters, have the same postjunctional effect so that there is a reinforcement of their individual effects;
- Opposite actions, which may result from a transmitter having opposite actions in different effector cells, or the response may depend on the tone of the effector cell;
- Prolongation of effect, by which a neuromodulator may act on degradative enzymes, for example peptidases responsible for removal of neuropeptides from the junctional cleft, to prolong the time course of their effect;
-Trophic effects, by which a neurotransmitter may effect theee expression of another transmitter or receptor within a population of neurons (for example in ganglia) at the level of gene transcription.
All these mechanisms of control of neurotransmission reflect the versitility of the ANS.

Sensory-motor nerves. The importance of sensory-motor nerve regulation in many organs is recognized (p. 667). These afferent nerves run in motor fibres with their cell bodies in cranial and dorsal root ganglia. While many such nerves are purely sensory, certain primary afferent nerve fibres have been termed sensory-motor since they release transmitter from their peripheral endings during the axon reflex and have a motor rather than a sensory role (see p 965) (Maggi 1991). For many years the status of the sensory nerve in the autonomic nervous system has been debated but now it is recognized that sensory-motor nerve regulation is an important feature of autonomic control in the gut, lungs, heart, ganglia, and blood vessels.

Intrinsic circuitry. Recognition that many intrinsic ganglia contain integrative circuits and are capable of sustaining and modulating sophisticated local activities. Although the ability of the enteric nervous system to sustain local reflex activity independent of the CNS has been recognized for many years (Kosterlitz 1968), it has been generally assumed that the intrinsic ganglia in peripheral organs such as the heart, airways, and bladder consisted of parasympathetic neurons that provided simple nicotinic relay stations. The high degree of electrophysiological specialization displayed by these intrinsic neurons suggests that they may act as sites of integration and/or modulation of the input from extrinsic nerves or permit some local control of aspects of visceral function by local reflex mechanisms (Allen & Burnstock 1990). Thus, since intrinsic neurons survive following section of the extrinsic sympathetic and parasympathetic nerves, transplanted organs are not denervated. Intrinsic neurons are derived from the neural crest, independent of sympathetic and parasympathetic nerves. Various combinations of transmitters have been shown to coexist in subpopulations of intrinsic neurons in atria, bladder and trachea and in the chemical coding in the enteric nervous system has been studied extensively (Furness & Costa 1987, p 1749).

Autonomic neuromuscular junction. Recognition that the autonomic neuromuscular junction differs in several important ways from the skeletal neuromuscular junction and from the synapses in the CNS and PNS (see Burnstock 1981). There is no fixed junction with well defined pre- and postjunctional specializations. Unmyelinated, highly branched, postganglionic autonomic nerve fibres reaching the effector smooth muscle become beaded or varicose (8.394). These varicosities are not static but are able to move along axons, consistent with the lack of postjunctional specialization. They are packed with mitochondria and vesicles containing neurotransmitters. The distance of the cleft between the variscosity and smooth muscle varies considerably depending on the tissue, from 20 nm in densely innervated structures such as the vas deferens to 1-2 um in large elastic arteries. Neurotransmitter is released en passage from variscosities during conduction of an impulse along an autonomic axon; however, it is possible that a given impulse will evoke release from only some of the variscosities that it encounters.

Another important feature of the autonomic neuromuscular junction is that, unlike striated muscle, the effector tissue is a muscle bundle rather than a single cell and low resistance pathways between individual muscle cells allow electronic coupling and spread of activity within the effector bundle. These are represented by areas of close apposition between the plasma membranes of adjacent cells which can be identified under the electron microscope as gap junctions or nexuses (p 958). Gap junctions vary in size from punctate junctions to junctional areas of more than 1 um in diameter. Little is known about the quantity and arrangement of gap junctions in effector bundles relative to the density of autonomic innervation. Thuis, within an effector muscle bundle only a certain percentage of cells are directly innervated, the remainder being coupled to these cells via gap junctions (Hillarp 1959; Burnstock 1986).

Plasticity. Recognition of the plasticity of the ANS, not only in normal development and ageing, but also in changes in the expression of neurotransmitters and receptors in the mature adult in response to hormones and growth factors following trauma, surgery, chronic drug treatment, and in a variety of disease situations (Burnstock 1990, p 959). Figure 8.394 is a depiction of an autonomic neuron with variscosities.

Next, more on the plasticity of the ANS.

[Diane]

P 1295 Gray's: PLASTICITY OF THE AUTONOMIC NERVOUS SYSTEM
Autonomic neuroeffector systems show a high degree of plasticity, even in mature adult animals (see Black et al 1988; Burnstock 1990; Hendry & Hill 1992). Changes in expression of transmitters and cotransmitters in autonomic nerves occur during developing and ageing, after chronic exposure to drugs, in a number of disease situations and in nerves that remain following trauma or surgery. Several different types of adaptive mechanisms appear to override the normal genetic programming of transmitter and receptor expression, for example alteraons in availability to growth factors, levels of nerve activity, removal of inhibitory innervation and hormonal changes. Neurotrophins synthesized by target smooth muscle, of which nerve growth factor is the best known example (Levi-Montalcini & Angelletti 1968; Thoenen 1991, p 919), have long been recognized to have trophic influences on sympathetic and sensory nerves of the autonomic nervous system. There is growing evidence that several neurotransmitters, in particular the neuropeptides, which are involved in short-term communication between excitable cells, also have long-term trophic actions on autonomic nerves (Pincus et al 1992). Autonomic neurons are thus continually under the influence of the molecules of their environment, allowing for a considerable degree of plasticity following injury (Hendry & Hill 1992).

Degeneration in the autonomic nervous system resembles that in cerebrospinal nerves. Some evidence suggests that the rate of degeneration differs in different regions or different types of fibre. Regeneration of preganglionic fibres may vary with the site of lesion and, in postganglionic neurons, regeneration may be followed by reinnervation from neighbouring intact nerve fibres. As far as experimental evidence goes, the integrity of Schwann cell sheaths is essential in the regeneration of autonomic nerve fibres (Evans & Murray 1954; Kapeller & Mayor 1967; Williams 1971; King & Thomas 1971; Landon 1976). Some observations suggest that proximity of myelinated fibres is necessary for regeneration in non-myelinated fibres (Evans & Murray 1954; Williams 1971; Lisney 1989; consult Fawcett & Keynes 1990). It is pertinent to mention earlier experiments in which large experimental gaps in the sympathetic trunk, in monkeys and other mammals, have been filled by the growth of fibres, pre- or postganglionic (Tower & Richter 1931; Haxton 1954). Functional recoveries may sometimes be explained by incomplete interruption of the sympathetic supply or by alternative routes being overlooked.
Next, surgical anatomy.

[Diane]

P 1296 Gray's: Surgical anatomy. Various autonomic nervous structures are divided or removed in treating several pathological conditions. In operations on the efferent sympatetic paths, ganglia on the sympathetic trunk are removed or preganglionic fibres cut, rather than postganglionic fibres, since the latter may regenerate. For example, the arteries of limbs may be denervated to alleviate vascular spasm (Raynaud's disease) and the parts removed are as described above (pp. 1258, 1302). In the treatment of hypertension, more extensive sympathectomy has been performed, involving bilateral removal of the sympathetic trunks from the eighth thoracic to the first lumbar ganglia, including the greater and lesser thoracic splanchnic nerves. Sympathectomy is also performed to relieve pain, for example in severe angina pectoris (p. 1311). Division of the superior hypogastric plexus (presacral neurectomy) does not relieve all pain in disease of the pelvic organs, because many pain fibres traverse the pelvic splanchnic nerves. However uterine pain fibres pass in sympathetic nerves via the superior hypogastric plexus so that this division does relieve dysmenorrhoea. In males resection of the superior hypogastric plexus leads to loss of ejaculation and sterility, due to interruption of the sympathetic paths to the seminal vesicles, deferent ducts and prostate. The routes of these nerves between the sympathetic ganglia and the superior hypogastric plexus are uncertain and may vary; but in some individuals an outflow from the first lumbar and possibly the twelfth thoracic ganglia is concerned and in others fibres from the third lumbar ganglion (White et al 1952).
Yikes.

Next, Parasympathetic NS. Nice big section, a full page. After that, the Sympathetic NS has its very own section, twelve pages long! We'll be lovingly delving into every ganglion known to humanity, if you can stick with this.

[Diane]

P 1297 Gray's:PARASYMPATHETIC NERVOUS SYSTEM
EFFERENT PATHWAYS
Preganglionic parasympathetic axons are myelinated and occur in the oculomotor, facial, glossopharyngeal, vagal, and accessory cranial nerves and in the second to fourth sacral spinal nerves. In the cranial part of the parasympathetic system there are four small peripheral ganglia: cilliary (p 1228), pterygopalatine (p. 1235), submandibular (p. 1247) and otic (p. 1250), all described in this account with their cranial nerves. These are soley efferent parasympathetic ganglia, unlike the trigeminal, facial, glossopharyngeal and vagal ganglia, all of which are concerned exclusively with afferent impulses and contain the somata of sensory neurons only. The cranial parasympathetic ganglia are traversed by afferent fibres, postganglionic sympathetic fibres and, in the otic, even by branchial efferent fibres, but none of these are interrupted in the ganglia. Postganglonic parasympathetic fibres are usually non-myelinated and shorter than the sympathetic, since the ganglia in which they synapse are in or near the viscera they supply. Baumann and Gajisin (1975) have emphasized the occurrence of small subsidiary ganglia near those mentioned above, confirming reports by others; they also described minute ganglia at many other sites in fetal material, for example along the middle meningeal artery and in some petrosal nerves.

1. Oculomotor preganglionic parasympathetic fibres commence in the midbrain at the accessory oculomotor (Edinger-Westphal) nuclei (p. 1227) and travel in the nerve in its branch to the inferior oblique to reach the ciliary ganglion. There they synapse, the post-ganglionic fibres leaving in the short ciliary nerves which pierce the sclera to run forwards in the perchoroidal space to the ciliary muscle (p. 1328) and the sphincter pupillae (p. 1331). These postganglionic axons are thinly myelinated.

2. The facial nerve contains preganglionic parasympathetic axons of neurons with their somata in the superior salivatory nucleus (p. 1243), emerging from the medulla oblongata in the nervus intermedius. These fibres leave the main facial trunk above the stylomastoid foramen in the chorda tympani, which traverses the tympanic cavity to reach the lingual nerve (p 1246). Thus they are conveyed to the submandibular ganglion, in which arise postganglionic secretomotor fibres for the submandibular salivary gland. Some preganglionic fibres may synapse around cells in the hilum of the gland (pp 1693, 1698). Postganglionic secretomotor fibres for the sublingual gland continue in the lingual nerve from the submandibular ganglion (pp 1247, 1693). Stimulation of chorda tympani dilates the arterioles in both glands in addition to having a direct secretomotor effect. The facial nerve is also usually said to contain efferent parasympathetic lacrimal secretomotor axons, which travel in its greater petrosal ramus and in the nerve of the pterygoid canal, relaying in the pterygopalatine ganglion. Postganglionic axons are said to travel by the zygomatic nerve to the lacrimal gland (p. 1235) and by ganglionic branches to the nasal and palatal glands. Evidence refuting the zygomatic route has been reported by Ruskell (1971), who favors direct lacrimal rami from a retro-orbital plexus of parasympathetic branches from the pterygopalatine ganglion. Clinical evidence suggests that some facial parasympathetic fibres reach the paratid gland (Diamant & Wiberg 1965 and p. 1243).

3. The glossopharyngeal nerve contains preganglionic parasympathetic secretomotor fibres for the parotid gland. These start in the inferior salivatory nucleaus (p. 1250) and travel in the glossopharyngeal nerve and its tympanic branch. They traverse the tympanic plexus and lesser petrosal nerve to reach the otic ganglion where they relay, the postganglionic fibres passing by communicating branches to the auriculotemporal nerve, which conveys them to the parotid gland. Stimulation of the lesser petrosal nerve produces vasodilator and secretomotor effects.

4. The vagus nerve contains preganglionic parasympathetic fibres whoich arise in its dorsal nucleus (p. 1251) and travel in the nerve and its pulmonary, cardiac, oesophageal, gastric, intestinal, and other branches. Some cardiac parasympathetic fibres may originate from neurons in or near the nucleus ambiguus (p. 1021). The proportion of efferent parasympathetic fibres in the vagus varies at different levels but is small relative to its sensory and sensory-motor content. Efferent fibres relay in minute ganglia in the visceral walls. The disproportion in the numbers of preganglionic to postganglionic fibres is greater in the vagus than in other cranial nerves; this cannot as yet be explained. Cardiac branches slow the cardiac cycle, joining the cardiac plexuses (p. 1306) and relaying in ganglia distributed freely over both atria in the subepicardial tissue (10.59), terminal fibres being distributed to the atria and the atrioventricular (AV) bundle and concentrated around the SA and (to a lesser extent) the AV nodes. It has been claimed in the past that only through the latter can the vagi influence ventricular muscle (Cullis & Tribe 1913), although there is a sparse postganglionic parasympathetic innervation of the ventricles (Higgins et al 1973). The smaller branches of the coronary arteries are innervated mainly via the vagus; larger arteries, with a dual innervation, are chiefly supplied by sympathetic fibres (Wollard 1926; Lundberg et al 1983; Owman 1988). Pulmonary branches are motor to the circular non-striated muscle fibres of the bronchi and bronchioles and are therefore bronchoconstrictor; synaptic relays occur in the ganglia of the pulmonary plexuses. Gastric branches are secretomotor and motor to the non-striated muscle of the stomach, with the exception of the pyloric sphincter, which they inhibit. Intestinal branches have a corresponding action in the small intestine, caecum, vermiform appendix, ascending colon, right colic flexure, and most of the transverse colon; they are secretomotor to the gonads, motor to the intestinal muscular coats but inhibitory to the ileocaecal sphincter. The synaptic relays are situated in the myenteric (Auerbach's) and the submucosal (Meissner's) plexuses (p. 1747).

5. The anterior rami of the second, third, and often fourth sacral spinal nerves issue pelvic splanchnic nerves (8.381) to the pelvic viscera. These nerves unite with branches of the sympathetic pelvic plexuses. Minute ganglia occur at the points of union and in the visceral walls. In these ganglia the sacral preganglionic parasympathetic fibres relay synaptically.

The pelvic splanchnic nerves are motor to the muscle of the rectum and bladder wall but inhibitory to the vesical sphincter, supply vasodilator fibres to the penile and clitoridic erectile tissue and are probably vasodilator to the testes and ovaries and vasodilator (and possibly inhibitory ) to the uterine tubes and uterus (de Groat 1992). Filaments from the pelvic splanchnic nerves ascend in the hypogastric plexus to supply the sigmoid and descending colon, the left colic flexure and terminal transverse colon with visceromotor fibres (Telford & Stopford 1934; Mitchell 1935; Christenson et al 1984).

Next, the sympathetics in some involved detail.

[Diane]

P. 1298 Gray's: SYMPATHETIC NERVOUS SYSTEM
The sympathetic system includes the two ganglionated trunks and their branches. plexuses and subsidiary ganglia. It has a much wider distribution than the parasympathetic, for it innervates
- all sweat glands
- the arrectores pilorum
- the muscular walls of many blood vessels
- the heart
- lungs and respiratory tree
- the abdomino-pelvic viscera
- oesophagus
- muscles of the iris in the eye
- non-striated muscle of the urogenital tract, eyelids and elsewhere.

There are differences in the pattern of sympathetic innervation of different effector tissues; for example, visceral smooth muscles such as the vas deferens and iris receive a dense varicose nerve plexus throughout with close, 20 nm neuromuscular separations, while most blood vessels receive an innervation which is confined to the adventitial-medial border with neuromuscular separations often greater than 80 nm.

EFFERENT PATHWAYS
The preganglionic fibres are axons of somata in the lateral grey column of all the thoracic and the upper two or three lumbar spinal segments, where they form intermediomedial and intermediolateral neuronal groups (p. 980). The axons are myelinated, with diameters of 1.5 - 4 um, and emerge from the spinal cord through the ventral spinal roots, passing into the spinal nerves at the start of their ventral rami, which they soon leave in white rami communicantes, to join either the corresponding ganglia of the sympathetic trunks or their interganglionic segments. This outflow is confined to the thoracolumbar region, the white rami communicantes being restricted to these 14 pairs of spinal nerves, although a limited outflow in other spinal nerves has been suggested. Neurons like those in the lateral grey column exist at other levels of the cord above and below the thoracolumbar outflow (Mitchell 1953) and small numbers of their fibres issue in other ventral roots. Dorsal spinal roots may also contain vasodilator fibres. Reaching the sympathetic trunk, preganglionic fibres may behave in several ways:
1. They may synapse with neurons in the nearest ganglion.
2. They may traverse this, ascending or descending in the sympathetic chain to end in another ganglion; note however that preganglionic fibres do not divide into ascending and descending branches. A single preganglionic fibre may, through collateral and terminal branches, synapse with neurons in several ganglia or terminate in only one ganglion.
3. They may traverse the nearest ganglion, ascend or descend and, without synapsing, emerge in one of the medially-directed branches of the sympathetic trunk to end at synapses in the ganglia of autonomic plexuses (mainly situated in the midline, for example around the coeliac and mesenteric arteries, p. 1307). Occasionally preganglionic fibres relay in ganglia situated proximal to the sympathetic trunks; these 'intermediate ganglia' are most numerous on grey rami communicantes (see below) at cervical and lower lumbar levels; they may be of microscopic size and sometimes occur in ventral roots or trunks. More than one preganglionic fibre may synapse with a single postganglionic neuron (see below).

The nervi terminales (p. 1225) may be rostral extensions of the sympathetic system, containing efferent postganglionic fibres distributed to the blood vessels and glands of the nasal cavity, although this view has been challenged (Bojsen-Moller 1975).

The sympathetic ganglia include collections of cells on the sympathetic trunks, in the autonomic plexuses and the 'intermediate' ganglia; some ganglionic cells are dispersed in the plexuses. Originally ganglia on the trunks correspond numerically to the ganglia on the dorsal spinal roots (p. 1261); but adjoining ganglia may fuse and there are rarely more than 22 or 23 and sometimes fewer. Subsidiary ganglia in the major autonomic plexuses (e.g. coeliac, superior mesenteric ganglia, etc.) are derivatives of the ganglia of the trunks. The functional properties of sympathetic ganglia have been investigated extensively over many decades, their peripheral location providing a valuable means of studying interneuronal communication, as well as other aspects of neurobiology (for reviews of the earlier literature see p 1292; more recent accounts are given by Gabella (1976), Eranko (1978), Elfvin (1983) and Szurszewski and King (1989).

Next; Structure of the sympathetic ganglia.
Tip: Imagine all this horizontal, as if in a quadruped, spine/spinal cord at the top, aorta running along it beneath/next story below covered in regulatory nerve net, chain ganglia along it, then some more cross wiring/big ganglia suspended between aorta and the belly/gut tube/endodermic system below that, everything surrounded by a spherical body wall balloon that has 4 parallel legs protruding downward and a head sticking out from it. It's easier to see the logic in the hookups that way. At least it is for me. Oh, and the balloon has a sensitive second balloon surrounding it which is slidey over it.

[Diane]

P. 1298 Gray's:
Structure of sympathetic ganglia
The classic studies by Langley and his successors led to the view that the autonomic ganglia are relay stations, a concept largely corroborated by anatomical observation, although it was soon recognized that a minor fraction of the fibres traversed one or more ganglia without synapse, some being efferent fibres on route to another ganglion and others afferents from the viscera and glands. This concept remains substantially true but has been modified and extended by electron microscopy, neurohistochemistry and electrophysiology, for example a considerable variation in the ratio between pre-and postganglionic fibres has been found (consult Skok 1973). The superior cervical sympathetic ganglion, the most extensively studied, has ratios varying from 1:28 to 1:176 in different mammalian species (Billingsley & Ranson 1918; Samuel 1953; Ebbesson 1968). It has long been accepted that preganglionic axons may synapse with many postganglionic neurons for the wide dissemination and perhaps amplification of sympathetic activity, a characteristic not shared to the same degree by parasympathetic ganglia. Dissemination may be achieved by:

- multiple synapses of preganglionic nerve fibres
- the mediation of interneurons
- the diffusion within the ganglion of transmitter substances locally produced (paracrine effect) or by a local response to a substance produced elsewhere (endocrine effect).

There is evidence that all of these mechanisms are involved. The connective tissue capsule of each ganglion, continuous with the epineurium of its connecting rami, also extends as septa into the ganglion, the surrounding groups of neurons and their fibres. More delicate extensions of this stroma spread amongst the cells, each of which is surrounded by a collagenous intercellular matrix containing a few fibroblasts and many small vessels including capillaries. Satellite cells (amphicytes) encapsulate the somata of ganglionic neurons and their processes. Externally this thin sheath of satillite cells has a continuous basal lamina and the two elements screen neurons from contact with the ganglionic extracellular matrix. Neurons thus have direct access only to the internal faces of satellite cells, the two being separated only by a narrow perineurial space of 15-20 nm which is, however, linked to the extracapsular spaces by narrow channels between the satellite cells, providing possible routes for the movement of nerotransmitter and hormonal substances between the somata of neurons and the vascular compartment.

Attempts to classify the neurons of the sympathetic (and parasympathic) ganglia, often on inadequate criteria, have entailed disagreements and confusion. Most are multipolar, with somata ranging from 25-50 um in mankind; a smaller type of about 15-20 um, less angular in shape and present in much smaller numbers, is often clustered in groups (De Castro & Herreros 1945) and probably corresponds to 'small intensely flourescent' (SIF) cells (see below). Multipolar neurons display much more dendritic variation; according to McLachlan (1974) they have (in guinea pigs) a mean of 13 dendrites per cell. The complexity of these dendrites, especially those ramifying in the capsular perikaryal space, is greater in human ganglion cells. Dendritic glomeruli have been observed in many ganglia. In general ultrastructure these glomeruli resemble others (p. 934); clusters of small, granular vesicles, adrenergic in type, are dispersed superficially in the perikaryon and also in the dendrites, probably representing the storage of catacholomines. Ganglionic neurons receive many axodendritic synapses from preganglionic nerve fibres, the axosomatic synapses being less numerous. Each preganglionic fibre forms several synapses with several separate dendrites, providing a mechanism for the dissemination and/or amplification of neural signals. Post ganglionic fibres (see below) commonly arise from the initial stem of a large dendrite and produce few or no collateral neurites. So the signal gets amped up and modulated right in the ganglia, by the wiring pattern itself being recursive and by how molecules of substances from elsewhere can come in to affect the neurons in strategic places. Next, interneurons.

[Diane]

P 1299 Gray's:
The existence of interneurons in sympathetic ganglia has been amply confirmed (Williams 1967; Williams & Palay 1969; Libet & Owman 1974), consisting of the SIF cells identified in sympathetic ganglia in many mammals, including man (Eranko & Harkonen 1965; Jacobowitz 1970). Small chomaffin cells also occur in sympathetic ganglia, as recognized by Kohn in 1898. Coupland (1965a) amongst other modern workers, has ascribed them to all ganglia of the sympathetic trunk and to other sites in human neonatal material. The distinction between SIF cells and chomaffin cells appears uncertain in many accounts. The supposed two types have been identified in ganglia by separate techniques (chromaffin reaction and formalin-induced flourescence) which cannot be applied together to a single cell. In the sympathetic ganglia of rats (Santer et al 1975) SIF cells were found to be more numerous than chromaffin cells and their modes of distribution showed some differences. Both contain catecholamines, some possibly only enough to be revealed by the more sensitive formaldehyde-induced flourescence technique (Falck-Hillarp), whereas others may have sufficient to produce a positive chromaffin reaction (Gabella 1976). Both types may be interneurons (Santer et al 1975; Gabella 1976) Greegard and Kebabian (1974) have suggested that the SIF cells release dopamine, which is then bound by dopamine receptors on ganglionic neurons causing hyperpolarization via a cyclic AMP-dependent 'second messenger' system. In the ganglia of some species, two types of SIF cell have been described (Williams et al 1975): a minority, with long processes, end near ganglionic neurons and hence can be regarded as interneurons (Type I), while the more numerous Type II cells have shorter processes ending near blood vessels. In bovine superior cervical sympathetic ganglia, 24% of SIF cells were described as Type I and 20% were so described in cats. Although the secretory granules in Type I cells may act directly on ganglionic neurons, some SIF cells, presumably Type II, may secrete into local blood vessels (Poloyni et al 1977), exerting more distant effects. The functions of SIF cells in neurotransmission in sympathetic ganglia have been reviewed by Eranko (1978) and Szurszewski and King (1989), and quantification of numbers, dimensions and packing density of ganglionic neurons are reported by Gabella (1976).

The axons of the principal ganglionic cells are narrow, nonmyelinated postganglionic fibres, distributed to effector organs in various ways:

1. Those from a ganglion of the sympathetic trunk may return to the spinal nerve of preganglionic origin through a grey ramus communicans, usually joining the nerve just proximal to the white ramus, to be distributed through ventral and dorsal spinal rami to blood vessels, sweat glands, hairs etc., in their zone of supply. Segmental areas vary in extent and overlap considerably. The extent of innervation of different effector systems, for example vasomotor, sudomotor etc., by a particular nerve may not be the same.

2. Postganglionic fibres may pass in a medial branch of a ganglion direct to particular viscera.

3. They may innervate adjacent blood vessels or pass along them externally to their peripheral distribution.

4. They may ascend or descend before leaving the sympathetic trunk as 1., 2., or 3. Many fibres are distributed along arteries and ducts as plexuses to distant effectors.

Fusion of grey and white rami may also occur, for example in the thoracic region; grey rami may also contain fasiculi of thick myelinated fibres which are somatic efferents using a grey ramus to reach the paravertebral muscles (see below), for example in the cervical region. For details of rami communicantes and their variations consult Winckler (1961). Next, functional significance.

[Diane]

P. 1300 Gray's: Functional significance
Postganglionic fibres which return to the spinal nerves supply vasoconstrictor fibres to blood vessels, are secretomotor to sweat glands and motor to the arrectores pilorum in their dermatomes. Those which accompany the motor nerves to peripheral nerves contain post-ganglionic sympathetic fibres. Those reaching the viscera are concerned with general vasoconstriction, bronchial and bronchiolar dilation, modification of glandular secretion, pupillary dilation, inhibition of alimentary muscle contraction, etc. A single preganglionic fibre probably synapses with the postganglionic neurons in only one effector system; hence effects such as sudomotor and vasomotor actions can be separate. This is not necessarily true of visceral afferent fibres.

Higher autonomic control
Peripheral autonomic activity is integrated at higher levels in the brainstem and cerebrum, including various nuclei of the brainstem reticular formation, thalamus, and hypothalamus, the limbic lobe and prefrontal cortex, together with the ascending and descending pathways which interconnect these regions (see details of these given earlier in this section). It is now recognized that central control of the cardiovascular system is exerted by a longitudinally arranged series of parallel pathways involving specific regions of the neuraxis extending from cerebral cortex to spinal cord (Loewry & Spyer 1990).

The sympathetic trunks are two ganglionated, irregular nerve cords extending from the cranial base to the coccyx. In the neck each lies posterior to the carotid sheath and anterior to the cervical transverse processes; in the thorax each is anterior to the heads of the ribs, in the abdomen anterolateral to the lumbar vertebral bodies and in the pelvis anterior to the sacrum and medial to the anterior sacral foramina. Anterior to the coccyx the two trunks meet in the single, median, terminal gangion impar.

Cervical sympathetic ganglia are usually reduced to three by fusion; from the cranial pole of the superior ganglion issues the internal carotid nerve, as a continuation of the sympathetic trunk, acompanying the internal carotid artery though its canal into the cranial cavity. There are from 10-12 (usually 11) thoracic ganglia, four lumbar and four or five in the sacral region.

Next: CRANIAL PART OF THE SYMPATHETIC SYSTEM

[Diane]

In the interests of keeping threads on select topics all linked together:
So what is it about the ANS we should know if we're dealing with skin? With pain? (http://www.somasimple.com/forums/showthread.php?p=17024#post17024)
Another link to an article (http://www.somasimple.com/forums/showthread.php?t=2496#post18943) on autonomics and headache.

After a bit of a break, back to Gray's, page 1300:
CRANIAL PART OF THE SYMPATHETIC SYSTEM
This begins on each side as the internal carotid nerve, a branch of the superior cervical ganglion containing the postganglionic fibres of its neurons. Ascending behind the internal carotid artery it divides in the carotid canal into branches, one medial and the others lateral to the artery. The larger, lateral branch gives filaments to the internal carotid and forms the lateral part of the internal carotid plexus; the medial branch also gives filaments to the artery and, continuing on, forms the medial part of the internal carotid plexus.

Internal carotid plexus
This surrounds its artery and occasionally contains a small medial carotid ganglion; elsewhere it has some scattered postganglionic neurons. Laterally the plexus communicates with the trigeminal and pterygopalatine ganglia, the adducent nerve and tympanic branch of the glossopharyngeal; it also distributes filaments to the wall of the internal carotid artery. One or two filaments join the adducent nerve as it lies on the lateral side of the internal carotid artery. The branch to the pterygopalatine ganglion is the deep petrosal nerve, which perforates the cartilage filling the foramen lacerum and forms with the greater petrosal nerve the nerve of the pterygoid canal, traversing the canal to the pterygopalatine ganglion. The communication with the tympanic branch of the glossopharyngeal nerve is effected by the superior and inferior caroticotympanic nerves in the posterior wall of the carotid canal.

The medial part of the internal carotid plexus is inferomedial to the part of the internal carotid artery which indents the cavernous sinus lateral to the sella turcica; it gives branches to the artery and to the oculomotor, trochlear, ophthlamic and abducent nerves and the ciliary ganglion. It also sends vasomotor rami along branches of the internal carotid to the hypohysis cerebri (p. 1887).

The branch to the oculomotor nerve joins the nerve near its point of division and the branch to the trochlear joins it in the lateral wall of the cavernous sinus; filaments also connect with the medial side of the ophthalmic nerve and with the abducent. The filament to the ciliary ganglion, from the anterior part of the plexus, enters the orbit via the superior orbital fissure; this ramus may join the ciliary ganglion directly or unite with the communicating branch from the nasociliary nerve (p. 1228); or it may travel in the ophthalmic nerve and its nasociliary branch. Its fibres traverse the ganglion without synapsing and enter the short ciliary nerves to be distributed to the blood vessels of the eyeball. Fibres supplying the dilator pupillae usually travel via the ophthalmic, nasociliary and long ciliary nerves but occasionally via the short ciliary. Some fibres may also innervate the ciliaris muscle. The preganglionic fibres concerned leave the spinal cord predominantly in T1, pass to and through the cervicothoracic ganglion and ascend in the cervical sympathetic trunk to relay in the superior cervical ganglion.

The internal carotid plexus is prolonged around the anterior and middle cerebral arteries and the ophthalmic arteries, reaching the pia mater along the cerebral vessels; along the ophthalmic artery they pass into the orbit where the plexus accompanies each branch of that vessel. Filaments on the anterior communicating artery connect the sympathetic nerves of the right and left sides and may be associated with a small ganglion. Much of this detail depends on rather old observations; continued disagreement and discrepancy have been reviewed by Mitchell (1953) and Purves (1972). Electron microscopy shows that the sympathetic innervation of the cerebral arterial tree is like that of other vascular systems and the terminals of this rich perivascular plexus have been shown histochemically and immunohistochemically to contain NA and NPY in various mammals, including man (Iwayama 1970; Matsuyama et al 1985). The sources of these sympathetic vasoconstrictor nerve fibres are the internal carotid and vertebral plexuses. It should be noted that, in cerebral vessels, some NPY-containing fibres are of parasympathetic origin, and also contain ACh- containing nerves present in some cerebral vessels after sympathectomy may be of central origin (Edvinsson 1991).

Next: Cervical part of the sympathetic system.

[Diane]

CERVICAL PART OF THE SYMPATHETIC SYSTEM
The cervical part of each sympathetic trunk contains three interconnected ganglia, the superior, middle and cervicothoracic which send grey rami communicantes to all the cervical spinal nerves but receive no white rami communicantes from them; their spinal preganglionic fibres emerge in the white rami communicantes of the upper thoracic spinal nerves which enter the corresponding thoracic sympathetic ganglia, through which they ascend into the neck. In their course, the grey rami communicantes may pierce the longus capitus or the scalenus anterior. For details of the cervical grey rami see Potts (1925), Pick and Sheehan (1946), Sunderland and Bedbrook (1949).

Superior cervical ganglion
This is the largest of the three, adjoins the second and third cervical vertebrae and is probably formed from four fused ganglia corresponding to C1-4. Anterior to it is the internal carotid artery and sheath, while posterior to it is the longus capitus. The internal carotid nerve (see above) ascends from it into the cranial cavity; the lower end of the ganglion is united by a connecting trunk to the middle cervical ganglion. Its branches consist of lateral, medial and anterior groups.

The lateral branches are the grey rami communicantes to the upper four cervical spinal nerves and to some of the cranial nerves; delicate filaments pass to the inferior vagal ganglion and to the hypoglossal nerve; a branch, the jugular nerve, ascends to the cranial base and divides into two, one part joining the inferior glossopharyngeal ganglion and the other the superior vagal ganglion; other twigs pass to the superior jugular bulb and associated jugular glomus or glomera and some to the meninges in the posterior cranial fossa.

The medial branches of the superior cervical ganglion are the laryngopharyngeal and cardiac. The laryngopharyngeal branches supply the carotid body and pass to the side of the pharynx, joining glossopharyngeal and vagal rami to form the pharyngeal plexus (p. 1252). A cardiac branch arises by two or more filaments from the lower part of the superior cervical gangion, occasionally receiving a twig from the trunk between the superior and middle cervical ganglia. It is thought to contain only efferent fibres, the preganglionic outflow being from the upper thoracic segments of the spinal cord, and to be devoid of pain (sic) fibres from the heart (p.1306). It descends behind the common carotid artery, in front of the longus colli, crossing anterior to the inferior thyroid artery and recurrent laryngeal nerve. The courses on the two sides then differ. The right cardiac branch usually passes behind or sometimes in front of the subclavian artery and posterolateral to the brachiocephalic trunk to the back of the aortic arch where it joins the deep (dorsal) part of the cardiac plexus. It has other sympathetic connections: about midneck it receives filaments from the external laryngeal nerve; inferiorly, one or two vagal cardiac branches join it; as it enters the thorax it is joined by a filament from the recurrent laryngeal nerve. Filaments from the nerve also communicate with the thyroid branches of the middle cervical ganglion. The left cardiac branch, in the thorax, is anterior to the left common carotid artery and crosses in front of the left side of the aortic arch to reach the superficial (ventral) part of the cardiac plexus. Sometimes it descends on the right of the aorta to end in the deep (dorsal) part of the cardiac plexus. It communicates with the cardiac branches of the middle cervical and cervicothoracic sympathetic ganglia and sometimes with the inferior cervical cardiac branches of the left vagus; branches from these mixed nerves form a plexus on the ascending aorta.

The anterior branches of the superior cervical ganglion ramify on the common and external carotid arteries and the branches of the latter, forming a delicate plexus around each in which small ganglia are occasionally found. The plexus around the facial artery supplies a filament to the submandibular ganglion; the plexus on the middle meningeal artery sends one ramus to the otic ganglion and another the external petrosal nerve, to the facial ganglion. Many of the fibres coursing along the external carotid and its branches ultimately leave them to travel to facial sweat glands via trigeminal nerve branches.

Next, middle cervical ganglion.

[Diane]

P. 1302 Gray's: Middle cervical ganglion
This is the smallest of the three. It is occasionally absent and may then be replaced by minute ganglia in the sympathetic trunk or may be fused with the superior ganglia. It is usually found at the sixth cervical vertebral level, anterior or just superor to the inferior thyroid artery, or it may adjoin the cervicothoracic ganglion (see below); it is probably a coalescence of the ganglia of the fifth and sixth cervical segments, judging by its postganglionic rami, which join the fifth and sixth cervical spinal nerves but sometimes also the fourth and seventh. The ganglion also has thyroid and cardiac branches. It is connected to the cervicothoracic ganglion by two or more very variable cords: the posterior usually splits to enclose the vertebral artery; the anterior loops down anterior to and then below the first part of the subclavian artery, medial to the origin of its internal thoracic branch, and supplies rami to it. This loop is the ansa subclavia; it is frequently multiple, lies closely in contact with the cervical pleura and generally connects with the phrenic nerve. Similar connections with the vagus nerve are of uncertain significance.

Thyroid branches accompany the inferior thyroid artery to the thyroid gland, communicating with the superior cardiac, external laryngeal and recurrent laryngeal nerves, and send branches to the parathyroid glands. Fibres to both glands are in part vasomotor but some reach the secretory cells (Raybuck 1952).

The cardiac branch, the largest sympathetic cardiac nerve, either arises from the ganglion itself or caudal to it. On the right side it descends behind the common carotid artery, in front of or behind the subclavian, to the trachea where it receives a few filaments from the recurrent laryngeal nerve before joining the right half of the deep (dorsal) part of the cardiac plexus. In the neck, it connects with the superior cardiac and recurrent laryngeal nerves. On the left side the cardiac nerve enters the thorax between the left common carotid and subclavian arteries to join the left half of the deep (dorsal) part of the cardiac plexus. Fine branches from the middle cervical ganglion also passs to the trachea and oesophagus.

I didn't know before that the vertebral artery usually tunnels through the posterior cord connecting the MCG to the next one down, the cervicothoracic.

[Diane]

P 1303 Gray's:
Cervicothoracic (stellate) ganglion
This is irregular in shape and much larger that the middle cervical ganglion. It is probably formed by a fusion of the lower two cervical and first thoracic segmental ganglia, sometimes including the second and even third and fourth thoracic ganglia. The first thoracic ganglion may be separate, leaving an inferior cervical ganglion above it. The sympathetic trunk turns backwards at the junctions of the neck and thorax and so the long axis of the cervicothoracic ganglion becomes almost anteroposterior. The ganglion lies on or just lateral to the lateral border of the longus colli between the base of the seventh cervical transverse process and the neck of the first rib (which are posterior to it), the vertebral vessels being anterior. Below it is separated from the posterior aspect of the cervical pleura by the suprapleural membrane; the costocervical trunk branches near its lower pole. Lateral is the superior intercostal artery.

A small vertebral ganglion may be present on the sympathetic trunk anterior or anteromedial to the origin of the vertebral artery and directly above the subclavian. When present, it may provide the ansa subclavia and is joined to the cervicothoracic ganglion by fibres enclosing the vertebral artery. It is usually regarded as a detached part of the middle cervical or cervicothoracic ganglion. Like the middle cervical ganglion it may supply grey rami communicantes to the fourth and fifth cervical spinal nerves. The cervicothoracic ganglion sends grey rami communicantes to the seventh and eighth cervical and first thoracic spinal nerves and gives off a cardiac branch, branches to nearby vessels and sometimes a branch to the vagus nerve.

The grey rami communicantes to the seventh cervical spinal nerve vary from one to five; two, the usual number, are shown in 8.398, 399. A third often ascends medial to the vertebral artery in front of the seventh cervical transverse process, connects with the seventh cervical nerve and sends a filament upwards through the sixth cervical transverse foramen in company with the vertebral vessels to join the sixth cervical spinal nerve as it emerges from the intervertebral foramen. An inconstant ramus may traverse the seventh cervical transverse foramen. Grey rami to the the eighth cervical spinal nerve vary from three to six in number.

The cardiac branch descends behind the subclavian artery and along the front of the trachea to the deep cardiac plexus. Behind the artery it connects with the recurrent laryngeal nerve and the cardiac branch of the middle cervical ganglion, the latter often being replaced by fine branches of the cervicothoracic ganglion and ansa subclavia.

Branches to blood vessels form plexuses on the subclavian artery and its branches. The subclavian supply is derived from the cervicothoracic ganglion and ansa subclavia, extending to the first part of the axillary artery; a few fibres may extend further. According to Pearson and Sauter an extension of the subclavian plexus to the internal thoracic artery is joined by a branch of the phrenic nerve (p. 1265). The vertebral plexus is derived mainly from a large branch of the cervicothoracic ganglion which ascends behind the vertebral artery to the sixth transverse foramen, reinforced by branches of the vertebral ganglion or the cervical sympathetic trunk which pass cranially on the ventral aspect of the artery; from this plexus deep rami communicantes join the ventral rami of the upper five or six cervical spinal nerves. The plexus contains some neuronal cell bodies and continues into the skull along the vertebral and basilar arteries and their branches as far as the posterior cerebral artery, where it meets a plexus from the internal carotid. Some consider the vertebral plexus to be the main intracranial extension of the sympathetic system (Lazorthes 1949; Mitchell 1952). The plexus on the inferior thyroid artery reaches the thyroid gland, connecting with recurrent and external laryngeal nerves, the cardiac branch of the superior cervical ganglion, and the common carotid plexus.

The preganglionic fibres for the head and neck emerge from the spinal cord in the upper five thoracic spinal nerves (mainly the upper three), ascending in the sympathetic trunk to synapse in the cervical ganglia. The preganglionic fibres supplying the upper limb stem from upper thoracic segments, probably T2-6 (or 7), ascending via the sympathetic trunk to synapse mainly in its cervicothoracic ganglion, whence postganglionic fibres pass to the brachial plexus (mainly its lower trunk). Most of the vasoconstrictor fibres for the upper limb emerge in the second and third thoracic ventral roots; the arteries can thus be denervated by cutting the sympathetic trunk below the third thoracic ganglion, severing the rami communicantes connected with the second and third thoracic ganglia or by cutting the ventral roots of the second and third thoracic spinal nerves (intradurally). The white ramus to the cervicothoracic ganglion is not cut, partly because it does not convey many vasomotor or sudomotor fibres to the upper limb but mainly because it contains most of the preganglionic fibres for the head and neck; these ascend the trunk to the superior cervical ganglion, from which postganglionic branches supply vasoconstrictor and sudomotor nerves to the face and neck, secretory fibres to the salivary glands, dilator pupillae (and probably cilaris oculi), non-striated muscle in the eyelids and the orbitalis. Destruction of this nerve would thus lead to meiosis, ptosis, enopthalmos and loss of sweating on the face and neck (Horner's syndrome) and possibly some disturbance of accomodation. For a review consult Haxton (1954) and Bannister and Mathias (1992).

Blood vessels of the upper limb beyond the first part of the axillary artery receive their sympathetic supply via branches of the brachial plexus adjacent to them, e.g. the median nerve supplies branches to the brachial artery and palmar arches, the ulnar nerve supplies the ulnar arery and palmar arches and the radial nerve supplies the radial artery.

The first and second (and occasionally the third) intercostal nerves may be interconnected anterior to the necks of the ribs by filaments containing postganglionic fibres from their grey rami; these fibres provide another path by which postganglionic nerves can pass from the upper thoracic ganglia to the brachial plexus.

Why anyone would want to manipulate all this I have no idea. Wait a minute, I do... by pretending that none of it exists in that moment in time, in the neck within one's hands? Sorry, it doesn't all go away just because you close your mind to its existence. You can't wish it away. It's going to be there whatever you do to someone's neck, so start learning less violent ways of treating it.

Next, the thoracic part of the sympathetic system.

[aléa]

P 1303 Gray's:


Why anyone would want to manipulate all this I have no idea. Wait a minute, I do... by pretending that none of it exists in that moment in time, in the neck within one's hands? Sorry, it doesn't all go away just because you close your mind to its existence. You can't wish it away. It's going to be there whatever you do to someone's neck, so start learning less violent ways of treating it.

Next, the thoracic part of the sympathetic system.

Can you imagine that therapists do know that ? Can you imagine osteopathy, or chiro, as a reflex therapy ? How do you think manipulations work ?

Saying that, I'm not a manipulation fanatic.

[Diane]

Alea, let me be clear that when I used the term "manipulation" I was referring to HVLA thrust type cracking. I'm not at all opposed to "handling" of the neck. I understand reflexive treatment fairly well, I think. Thank you for your input.

[Barrett Dorko]

Diane,

I think the work you've done here should be required reading in every PT program.

In my experience, (years of that every day) manipulation doesn't result in much of anything - no increase in range, no change in symptoms. Every once in a great while people would be briefly better, sometimes worse. There was no predicting any of this.

There's a discussion on RE about the persistance of symtomotology after "whiplash." Various studies indicate that these aren't just driven by financial considerations. It seems that the anatomical reality of the region and its connection to the possibility of physiologic irritation is something that should always be considered.

It seems to me that the neck's typical lack of response to manipulation is a testament to its adaptability.

[Diane]

The neck is an interesting place
1. with all this essential wiring to vital food intake structures and airways and balance/equilibrium function;
2. vital tubing (vessels) and cord (to rest of body);
3. given the fact that embryologically the diaphragm and heart start out in there and that maybe part of the brain still thinks they are in there;
4. given the fact that even if it is strained, say in a whiplash accident, it still has to support the head? i.e., no way to rest it other than lay it down, or immobilize it in a collar (shown to be couterproductive for all sorts of reasons);
5. given the above, is it any wonder the brain may feel more greatly threatened when the neck is injured in, say, whiplash, in terms of a persistent pain state in the neck representation, than if, say, in a knee representation if a knee is dinged on the dashboard in the same accident?

Anyway, moving on to another interesting bit:
P. 1303, Gray's:
THORACIC PART OF THE SYMPATHETIC TRUNK
The thoracic sympathetic trunk contains ganglia almost equal in number to those of the thoracic spinal nerves (11 in more than 70%, occasionally 12, rarely 10 or 13). The first thoracic ganglion is usually fused with the inferior cervical, forming the cervicothoracic ganglion; Jit and Mukerjee (1960) found a fused ganglion in 80 out of 100 dissections. Rarely the middle cervical or second thoracic ganglion may be included. The succeeding ganglion is counted as the second in order to make the other ganglia correspond numerically with other segmental structures. Except for the lowest two or three the thoracic ganglia lie against the costal heads, posterior to the costal pleura; the lowest two or three are lateral to the bodies of the corresponding vertebrae. Caudally, the thoracic sympathetic trunk passes dorsal to the medial arcuate ligament (or through the crus of the diaphragm) to become the lumbar sympathetic trunk. The ganglia are small and interconnected by intervening segments of the trunk. Two or more rami communicantes, white and grey, connect each ganglion with its corresponding spinal nerve, white rami joining the nerve distal to the grey. Sometimes a grey and white ramus fuse to form a 'mixed' ramus (p. 1298).

The medial branches from the upper five ganglia are very small, supplying filaments to the thoracic aorta and its branches. On the aorta they form a fine thoracic aortic plexus with filaments from the greater splanchnic nerve. Rami of the second to fifth or sixth ganglia enter the posterior pulmonary plexus; others, from the second to fifth ganglia, pass to the deep (dorsal) part of the cardiac plexus. Small branches of these plumonary and cardiac nerves pass to the oesophagus and trachea. The medial branches from the lower seven ganglia are large, supplying the aorta and uniting to form the greater, lesser and lowest splanchnic nerves, the last not always being identifiable.

The greater splanchnic nerve consisting mainly of myelinated preganglionic efferent and visceral afferent fibres, is formed by branches from the fifth to ninth or tenth thoracic ganglia; but fibres in the upper branches may be traced to the first or second thoracic ganglion. Its roots vary from one to eight, four being the most usual number. It descends obliquely on the vertebral bodies, supplies branches to the descending thoracic aorta and perforates the ipsilateral crus of the diaphragm to end mainly in the coeliac ganglion but partly in the aortorenal ganglion and suprarenal gland. A splanchnic ganglion exists on the nerve opposite the eleventh or twelfth thoracic vertebra in 17-68% of dissections (Jit & Mukerjee 1960); but Mitchell (1953) reported microscopic evidence that it is always present.

The lesser splanchnic nerve formed by rami of the ninth and tenth (sometimes tenth and eleventh) thoracic ganglia and the trunk between them, pierces the diaphragm with the greater splanchnic to join the aorticorenal ganglion.

The lowest (least) splanchnic nerve (or renal nerve) from the lowest thoracic ganglion enters the abdomen with the sympathetic trunk to end in the renal plexus.

Jit and Mukerjee (1960) described in great detail dissections of the thoracic sympathetic nerves in 50 cadavers and surveyed the previous findings. The incidence of the splanchnic nerves, according to seven observers, is as follows: greater - always present, lesser - 94% (86-100%), least - 56% (16-98%). A fourth (accessory) splanchnic nerve has been described by deSousa (1955) but has not been confirmed.

With all this vital wiring piercing the diaphgram I would be inclined to predict that the "green light" types delineated on Nick's mechanical peripheral NS deformation thread lately, who can't abdominally breath and whose spines seem so rigid would maybe be nonconsciously guarding/defending their sympathetic chains. I wonder if the postural restoration people have looked into sympathetic nervous system anatomy, reflected on it, allowed it to inform their thinking to any extent?

:note2: "(Ooh! Uh! ooh! uh!)
Hey don't you know..
That's the sound of the men..
Working on the chain...
Ganglia.." :note:

[Diane]

P 1304 Gray's:
LUMBAR PART OF THE SYMPATHETIC SYSTEM
The lumbar part of each sympathetic trunk usually containing four interconnected ganglia, runs in the extra-peritoneal connective tissue anterior to the verterbral column and along the medial trunk of the psoas major. Superiorly it is continuous with the thoracic trunk posterior to the medial arcuate ligament; inferiorly, passing posterior to the common iliac artery, it becomes the pelvic trunk. On the right side it is overlapped by the inferior vena cava and on the left by the lateral aortic lymph nodes. It is anterior to most of the lumbar vessels but may pass behind some lumbar veins.

The first, second and sometimes third lumbar ventral spinal rami send white rami communicantes to the corresponding ganglia. Grey rami communicantes passing from all ganglia to the lumbar spinal nerves, are long and accompany the lumbar arteries round the sides of the vertebral bodies, medial to the fibrous arches to which the psoas major is attached.

Usually four lumbar splanchnic nerves pass from the ganglia to join the coeliac, intermestenteric (abdominal aorta) and superior hypogastric plexuses. The first lumbar splanchnic nerve, from the first ganglion joins the coeliac, renal and intermestenteric plexuses. The second nerve, from the second and sometimes the third ganglion, joins the inferior part of the intermesenteric plexus; the third nerve issues from the third or fourth ganglion, passsing anterior to the common iliac vessels to join the superior hypogastric plexus. The fourth lumbar splanchnic, from the lowest ganglion, passes dorsal to the common iliac vessels to join the lower part of the superior hypogastric plexus or the hypogastric 'nerve'.

Vascular branches from all lumbar ganglia join the intermesenteric (aortic) plexus. Fibres of the lower lumbar splanchnic nerves pass to the common iliac arteries, forming a plexus continued along the internal and external iliac arteries as far as the proximal part of the femoral artery. Many postganglionic fibres in the grey rami, connecting the lumbar ganglia to the spinal nerves, travel in the femoral nerve to its muscular, cutaneous and saphenous branches, supplying vasoconstrictor nerves to the femoral artery and its branches in the thigh. Other postganglionic fibres travel via the obturator nerve to the obturator artery. Considerable uncertainties persist regarding sympathetic supplies to the lower limb (Wilde 1951; Wyburn 1956; Pick 1970).

Some of this bears repeating: Many postganglionic fibres in the grey rami, connecting the lumbar ganglia to the spinal nerves, travel in the femoral nerve to its muscular, cutaneous and saphenous branches, supplying vasoconstrictor nerves to the femoral artery and its branches in the thigh. Other postganglionic fibres travel via the obturator nerve to the obturator artery. Does anyone else see the possibilities here for eliciting positive reflex autonomic activity by handling skin on the front of the thigh? Up into the hip perhaps?

Next, pelvic part of the sympathetics.

[nari]

Yep, it certainly sounds likely that skin contact--> autonomic activity is logical. Could be hard to disprove...

Nari

[Diane]

P. 1305 Gray's:
PELVIC PART OF THE SYMPATHETIC SYSTEM
The pelvis sympathetic trunk lies in the extraperitoneal tissue anterior to the sacrum, medial or anterior to the anterior sacral foramina, and has four or five interconnected ganglia. Above, it continues into the lumbar trunk; below, the two trunks converge to unite in the small ganglion impar anterior to the coccyx. Grey rami communicantes pass from the ganglia to sacral and coccygeal spinal nerves but white rami communicantes are absent. Medial branches of distribution connect across the midline; twigs from the first two ganglia join the inferior hypogastric plexus (pelvic plexus) or the hypogastric 'nerve'; others form a plexus on the median sacral artery. The glomus coccygeum is supplied from the loop between the two trunks. The hypogastric 'nerve', which is usually plexiform, is a redundant term for the right and left connections, between the superior and inferior hypogastric plexuses (p. 1308).

Vascular branches
Through the grey rami many postganglionic fibres pass to the roots of the sacral plexus, especially those forming the tibial nerve, to be conveyed to the popliteal artery and its branches in the leg and foot. Others are carried in the poudendal and superior and inferior gluteal nerves to the accompanying arteries. Branches to the lymph nodes are also described (Wozniak 1966).

Preganglionic fibres for the lower limb are derived from the lower three thoracic and upper two or three lumbar spinal segments. They reach the lower thoracic and upper lumbar ganglia through white rami; some descend through the sympathetic trunk to synapse in the lumbar ganglia, whence postganglionic fibres join the femoral nerve to supply the femoral artery and its branches; other fibres descend to synapse in the upper two or three sacral ganglia, from which postganglionic axons join the tibial nerve to supply the popliteal artery and its branches in the leg and foot. Sympathetic denervation of vessels in the lower limb can thus be effected by removing the upper three lumbar ganglia and the intervening parts of the sympathtic trunk, all the preganglionic fibres to the lower limb thus being divided.

SEGMENTAL SYMPATHETIC SUPPLIES
Segmental sympathetic supplies are as follows: (Note: I reorganized the list to have it make sense embryologically. Nothing has been excluded or added.)

Head, neck, heart: T1-5
Bronchi and lung T2-4
Upper limb: T2-5
Oesophagus (caudal part) T5-6
Stomach, spleen, pancreas T6-10
Liver and gallbladder T7-9
Suprarenal T8-L1
Small intestine T9-10
Kidney T10-L1
Tests and ovary T10-11
Large intestine to splenic flexure, prostate, prostatic urethra T11-L1
Ureter, epididymis, ductus deferens, seminal vesicles, bladder T11-L2
Uterus T12-L1
Large intestine splenic flexure to rectum L1-2
Uterine tube T10-L1
Lower limb T10-L2

There. I'm sure the nervous system would rather have the list in the order I have put it in. :) The previous order was according to tissue systems; musculoskeletal, thoracic organs, GI tract etc..

Yeah, Gray's really did use the word "whence." Even in 1995. That is not a typo.

The big takeaway point for me is all the sympathetic fibres in the regular nerves. It has got to feel good (everywhere) to get them liberated from the surrounding mesoderm within the leg..

Next, plexuses in the thoracic, abdominal and pelvic cavities.

[Diane]

P 1306, Gray's
PLEXUSES IN THE THORACIC, ABDOMINAL, AND PELVIC CAVITIES
The larger autonomic plexuses are aggregations of nerves and ganglia situated in the thoracic, abdominal and pelvic cavities. They are the cardiac, plumonary, coeliac and hypogastric plexuses, supplying the thoracic, abdominal, and pelvic viscera, respectively. Extensions of these major plexuses pass along most branches of the large vessels which they surround and are usually named after the artery along which they are distributed. This leads to a plethora of named plexuses, often separately described in detail which may overshadow their essential unity.

CARDIAC PLEXUSES
The cardiac plexus at the base of the heart is divided into superficial (ventral) and deep (dorsal) parts which are closely connected. Several small ganglia lie within it, the most constant being the cardiac ganglion described below. Mizeres (1963) has emphasized the unity of the cardiac plexus, considering its division into two parts as an artefact of dissection; he was, however, prepared to allow regional names for its coronary, pulmonary, atrial and aortic extensions. Since major concentrations of the plexus are situated as described here, the terms superficial and deep have been retained.
More on the cardiac plexus next time.

[Diane]

P 1306 Gray's
Superficial (ventral) part of the cardiac plexus
This lies below the aortic arch and anterior to theright pulmonary artery. It is formed by the cardiac branch of the left superior cervical sympahetic ganglion and the lower of the two cervical cardiac branches of the left vagus. A small cardiac ganglion is usually present in this plexus immediately below the aortic arch, to the right of the ligamentum arteriosum. This part of the cardiac plexus connects with (1) the deep part, (2) the right coronary plexus, (3) the left anterior pulmonary plexus.

Deep (dorsal) part of the cardiac plexus
This is anterior to the tracheal bifurcation, above the point of division of the pulmonary trunk and posterior to the aortic arch. It is formed by the cardiac branches of the cervical and upper thoracic sympathetic ganglia and of the vagus and recurrent laryngeal nerves. The only cardiac nerves which do not join it are those joining the superficial part of the plexus.

Branches from the right half of the deep part of the cardiac plexus pass in front of and behind the right pulmonary artery; those anterior to it, the more numerous, supply a few filaments to the right anterior pulmonary plexus and continue on to form part of the right coronary plexus; those behind the pulmonary artery supply a few filaments to the right atrium and then continue into the left coronary plexus. Ther left half of the deep part of the cardiac plexus is connected with the superficial, supplying filaments to the left atrium and left anterior pulmonary plexus and then continuing to form much of the left coronary plexus.

Left coronary plexus
This is larger than the right, and is formed chiefly by the prolongation of the left half of the deep part of the cardiac plexus and a few fibres from the right; it accompanies the left coronary artery to supply the left atrium and ventricle.

Right coronary plexus
This is formed from both superficial and deep parts of the cardiac plexus, and accompanies the right coronary artery to supply the right atrium and ventricle.

Atrial plexuses
Described by Mizeres (1963), these are derivatives of the right and left continuations of the cardiac plexus along the coronary arteries. Their fibres are distributed to the corresponding atria, overlapping those from the coronary plexuses.

All the cardiac branches of the vagus and sympathetic contain both afferent and efferent fibres, except the cardiac branch of the superior cervical sympathetic ganglion, which is purely efferent. The efferent preganglionic cardiac sympathetic fibres arise in the upper four or five thoracic spinal segments; they pass by white rami communicantes to synapse in trhe upper thoracic sympathetic ganglia, though many ascend to synapse in the cervical ganglia. Post-ganglionic fibres from the thoracic and cervical ganglia form the sympathetic cardiac nerves, which accelerate the heart and dilate the coronary arteries. Of the sympathetic fibres from the first four or five thoracic spinal segments, the upper pass to the ascending aorta, pulmonary trunk and ventricles, the lower to the atria.

The efferent cardiac parasympathetic fibres from the dorsal vagal nucleus and neurons near the nucleus ambiguus run in vagal cardiac branches to synapse in the cardiac plexuses and atrial walls. These vagal fibres slow the heart and cause constriction of the coronary arteries (p. 1500). In man (like most mammals) intrinsic cardiac neurons are limited to the atria and interatrial septum (Davies et al 1952; King & Coakley 1958); they are most numerous in the subepicardial connective tissue near the SA and AV nodes. There is now evidence that these intrinsic ganglia are not simple nicotinic relays but may also act as sites for integration of extrinsic nervous inputs and form complex circuits for the local neuronal control of the heart and perhaps even local reflexes (consult Saffrey et al 1992).

Thus does the CNS remain aware of its own heart beating. The segmental sympathetic supplies to head neck AND heart, are T1-5. The heart started out in the neck and then the head and neck grew away from it.

Something I'd like to accomplish one fine day is to learn to (confidently) visualize the difference between white (http://anatomy.uams.edu/AnatomyHTML/introautonomics.html) and grey (http://anatomy.med.umich.edu/modules/intro_autonomics_2_module/autonomics_06.html) rami communicantes without all that complex wiring and function blurring together in my mind.

[Diane]

P 1307 Gray's:
PULMONARY PLEXUSES
These are anterior and posterior to the other hilar structures of the lungs, the anterior plexus being much smaller. According to Mizeres (1963) they are extensions from the cardiac plexus along the right and left pulmonary arteries. They are formed by vagal and sympathetic branches. Efferent parasympathetic fibres arise from the dorsal vagal nucleus; efferent sympathetic fibres are postganglionic branches of the second to fifth thoracic sympathetic ganglia.

The anterior plumonary plexus is formed by rami from vagal and cervical sympathetic cardiac nerves as well as direct branches from both sources; the posterior plumonary plexus is formed by the rami of vagal cardiac branches from the second to fifth or sixth thoracic sympathetic ganglia, the left plexus also receiving branches from the left recurrent laryngeal nerve. The two plexuses are interconnected; from them nerves enter the lung as networks along branches of the bronchi and pulmonary and bronchial vessels extending as far as the visceral pleura. There are small ganglia within the tracheobronchial tree of the airways with which efferent vagal preganglionic fibres synapse (Coburn 1987). They may act as sites of integration and/or modulation of the input from extrinsic nerves or permit some local control of aspects of airway function by local reflex mechanisms (Allen & Burnstock 1990). In the small intestine interstitial cells have been described in terminal autonomic networks, but have not been seen in thoracic organs, apart perhaps from the oesophagus (Dijkstra 1969). Efferent vagal fibres are bronchoconstrictor, secretomotor to bronchial glands and vasodilator. Efferent sympathetic fibres are bronchodilator and vasomotor. Lest we forget, the lungs bud off the foregut in the embryo. The esophagus and the trachea are originally one tube, that separates into two.

[Diane]

COELIAC PLEXUS
The coeliac, the largest major autonomic plexus, sited at the level of the last thoracic and first lumbar vertebrae, is a dense network uniting two large coeliac ganglia. It surrounds the coeliac artery and the root of the superior mesenteric artery. It is posterior to the stomach and omental bursa, anterior to the crura of the diaphragm and the commencement of the abdominal aorta and between the suprarenal glands. The plexus and ganglia are joined by the greater and lesser splanchnic nerves of both sides and branches from both the vagus and phrenic nerves. They extend as numerous secondary plexuses along adjacent arteries.

The coeliac ganglia are irregular masses, one on each side, between the suprarenal gland and the coeliac trunk and in front of the crura; the right one is behind the inferior vena cava, the left behind the splenic vessels. The upper part of each is joined by a greater splanchnic nerve; the lower part, more or less detached as the aroticorenal ganglion, receives the lesser splanchnic nerve and forms most of the renal plexus; its position is variable but near the origin of the renal artery from the aorta. (For details consult Norvell 1968). Secondary plexuses from or connected with the coeliac are: the phenic, splenic, hepatic, left gastric, intermesenteric, suprarenal, renal, testicular or ovarian, superior mesenteric and inferior mesenteric.

Phrenic plexus
This accompanies the inferior phrenic artery to the diaphragm, with branches to the suprenal gland. It arises near the upper end of the coeliac ganglion and is larger on the right. It receives one or two phrenic branches. At the junction of the right phrenic plexus with the phrenic nerve is a small [i]phrenic ganglion, distributing branches to the inferior vena cava, suprarenal and hepatic plexuses.

Hepatic plexus
The largest coeliac derivative, this also receives filaments from the left and right vagi and right phrenic nerve. It accompanies the hepatic artery and portal vein and their branches into the liver, where its fibres are confined to the vicinity of the blood vessels. It follows all branches of the hepatic artery. Branches to the gallbladder form a thin cystic plexus; bile ducts are also supplied. Branches accompanying the right gastric artery supply the pylorus. From the gastroduodenal extension of the plexus branches reach the pylorus and the first part of the duodenum. Many follow the right gastro-epiploic artery to supply the right side of the stomach and the greater curvature. The superior pancreaticoduodenal extension of the plexus supplies the descending part of the duodenum, the pancreatic head and the lower part of the bile duct. The hepatic plexus contains afferent and efferent sympathetic and parasympathetic fibres; the vagal constituents are said to be motor to the musculature of the gallbladder and bile ducts and inhibitory to the sphincter of the bile duct. Petkov (1968) identified a distinct nerve to the sphincter in 23 out of 25 human dissections.

Left gastric plexus
This accompanies its artery along the lesser curvature of the stomach, joining with the vagal gastric branches. Gastric sympathetic nerves are motor to the pyloric sphincter but inhibitory to the gastric mural musculature.

Splenic plexus
This is formed by branches of the coeliac plexus, left coeliac ganglion and right vagus, and accompanies its artery to the spleen, giving off subsidiary plexuses along arterial branches. The fibres are mainly, perhaps wholly, sympathetic and terminate in blood vessels and non-striatred muscle of the splenic capsule and trabeculae.

Suprarenal plexus
This is formed by branches from the coeliac ganglion and plexus and greater splanchnic nerve. Relative to its size, the suprarenal gland has a larger autonomic supply than any other organ. Its fibres are commonly described as myelinated and preganglionic. In rats, however, non-myelinated fibres are ten times as numerous and are considered preganglionic; they end in synapses, often deeply invaginated, with large chromaffin cells, the phaeochromocytes, which are thus homologous with the postganglionic sympathetic neurons (p.1905). A space of 150-200 nm separates the synaptic membranes, which often have electron-dense zones. Small and large vesicles with electron-dense granular contents occur in these endings. Only non-myelinated fibres appear to innervate chomaffin cells, all of which are related to one or more such terminals. Multi-polar neurons also occur in the adrenal medulla; some preganglionic non-myelinated fibres form axodendritic synapses with them. The destination of their axons is not known (Coupland 1965a). A preponderance of non-myelinated fibres has also been described in the human suprarenal plexus (Coupland 1965a, b; Grottel 1968).

Renal plexus
This is dense and formed by rami from the coeliac ganglion and plexus, aorticaorenal ganglion, lowest thoracic splanchnic nerve, first lumbar splanchnic nerve and aortic plexus. Small ganglia occur in the renal plexus, the largest usually behind the start of the renal artery. The plexus continues into the kidney around the arterial branches to supply the vessels, renal glomeruli, and tubules, especially the cortical tubules (Norvell 1968). Renal nerves are mostly vasomotor. From the renal plexus branches supply ureteric and tesicular (or ovarian) plexuses. The ureteric plexus receives, in its upper part, branches from the renal and aortic plexuses, in its intermediate part from the superior hypogastric plexus and hypogastric nerve and in its lower part from the hypogastric nerve and inferior hypogastric plexus. This supply influences the inherent motility of the ureter.

Testicular plexus
This accompanies the testicular artery to the testis. Its upper part receives branches from the renal and aortic plexuses. Distally it is reinforced from the superior and inferior hypogastric plexuses. Its rami pass to the epididymis and ductus deferens.

Ovarian plexus
This accompanies the ovarian artery to the ovary and uterine tube. The upper part is formed by branches from the renal and aortic plexuses; its lower part is reinforced from the superior and inferior hypogastric plexuses.

The nerves in the testicular and ovarian plexuses contain efferent and afferent sympathetic fibres; the efferents are vasomotor and derived from the tenth and eleventh thoracic spinal segments; the parasympathtic fibres, from the inferior hypogastric plexuses, are probably vasodilator.

Superior mesenteric plexus
This is a downward continuation of the coeliac, which receives a branch from the junction of the right vagus and coeliac plexus. It accompanies the superor mestenteric artery into the mesentery, dividiung into secondary plexuses distributed to parts supplied by the artery: pancreatic, jejunal and ileal, ileocolic, right colic, and middle colic. The superior mesenteric ganglion lies superior in the plexus, usually above the superior mesenteric artery's origin. Intestinal sympathetic nerves are motor to the ileocaecal sphincter but inhibitory to the mural musculature; some are vasoconstrictor.

Abdominal aortic plexus (intermesenteric plexus)
This is formed by branches from the coelic plexus and ganglia and receives rami from the first and second lumbar splanchnic nerves. It is on the sides and front of the aorta, between the origins of the superior and inferior mesenteric arteries. It consists of four to 12 intermesenteric nerves, connected by oblique branches. It is continuous above with the coeliac plexus and coeliac and aorticorenal ganglia, below with the superior hypogastric plexus. From it parts of testicular, inferior mesenteric, iliac, and superior hypogastric plexuses arise; it also supplies the inferior vena cava.

Inferior mesenteric plexus
This is chiefly from the aortic plexus but also from the second and lumbar splanchnic nerves. It surrounds the inferior mesenteric artery and is distributed along its branches; thus a left colic plexus supplies the left part of the transverse colon, the descending and the sigmoid colon; a superior rectal plexus supplies the rectum. Near the origin of the inferior mesenteric artery an inferior mesenteric ganglion may occur but more often small ganglia are scattered around the origin of the artery in the proximal part of the plexus. In one study (Southam 12959) an [i]inferior mesenteric ganglion occurred in all of 22 human stillborn infants. The colic sympathetic nerves are inhibitory to mural muscle in the colon and rectum. Branches from parasympathetic pelvic splanchnic nerves ascend occasionally through but usually near the superior hypogastric and inferior mesenteric plexuses to supply the large intestine from the left half of the transverse colon to the rectum (p. 1786); they are motor to the colic musculature. It is to be emphasized that the parasympathetic supply to the distal colon is largely by these direct branches of the pelvic splanchnic nerves, not via the hypogastric and inferior mesenteric plexuses (Mitchell 1935; Woodburne 1956).

Next, superior and inferior hypogastric plexuses.

[Diane]

P. 1308 Gray's
SUPERIOR HYPOGASTRIC PLEXUS
The superior hypogastric plexus is anterior to the aortic bifurcation, the left common iliac vein, medial sacral vessels, fifth lumbar vertebral body and sacral promontory and between the common iliac arteries. Often termed the presacral nerve it is seldom a single nerve, and is prelumbar rather than presacral. It lies in extraperitoneal connective tissue; the parietal peritoneum can easily be stripped off its anterior aspect. It varies in breadth and condensation of its constituent nerves and is often a little to one side of the midline (more often to the left); the attachment of the sigmoid mesocolon, containing superior rectal vessels, is to the left of the lower part of the plexus. Scattered neurons occur in it. The plexus is formed by branches from the aortic plexus and third and fourth lumbar splanchnic nerves. It divides into right and left hypogastric 'nerves' which descend to the two inferior hypogastric plexuses. The superior plexus supplies branches to the ureteric, testicular, ovarian and common iliac plexuses. In addition to sympathetic fibres, it may also contain parasympathetic fibres (from pelvic splanchnic nerves) which descend from the inferior hypogastric plexus; but these fibres usually ascend to the left of the superior hypogastric plexus and across the sigmoid branches of left colic vesssels. These parasympathetic fibres are distributed partly along the inferior mesenteric arterial branches and also as independent retroperitoneal nerves to supply the left part of the transverse colon, left colic flexure, descending and sigmoid colon.

I found a nice visual (http://anatomy.med.umich.edu/modules/pelvic_autonomic_module/pelvic_page12.html) for the autonomics. There is a click in the upper right to change views, but it only works in reverse, so start of page 12 and work backwards.

Enjoy.

I'm back in this post to announce that I found a small author error in the link I've placed here. On page 2 of 12, the author says (about visceral afferents) "These fibres, originating within the spinal cord, accompany visceral efferent fibres throughout their pathways." I'm here to say, that visceral afferent fibres do NOT originate within the spinal cord; rather they are from neural crest and therefore are more likely to "originate" as part of DRGs, same as all the rest of the sensory system. Only motor fibres originate in the cord. At least that's how I understand origins based on embryology.

[Diane]

P 1309, Gray's
INFERIOR HYPOGASTRIC PLEXUSES
The superior hypogastric plexus divides caudally into right asnd left hypogastric 'nerves', each descending in extraperitoneal connective tissue into the pelvis, medial to each internal iliac artery and its branches to become the inferior hypogastric plexus. Each nerve may be single or an elongated plexus of anastomosing filaments. (Hypogastric nerves can scarcely be distinguished from their continuations, the inferior hypogastric plexuses. The latter are joined by pelvic splanchnic nerves, a distinction minimized by the fact that both nerves and plexuses contain sympathetic and parasympathetic fibres. Some authorities prefer to describe a superior hypogastric plexus dividing into two inferior plexuses.) From each hypogastric nerve branches may pass to the testicular, ovarian and ureteric plexus or to the internal iliac plexuses and to the sigmoid colon; each nerve may be joined initially by the lowest lumbar splanchnic nerve from last lumbar sympathetic ganglion.

Inferior hypogastric (pelvic) plexus
This is in the extraperitoneal connective tissue. In males it is lateral to: the rectum, seminal vesicle, prostate and the posterior part of the urinary bladder. In females each plexus is lateral to: the rectum, uterine cervix, vaginal fornix and the posterior party of the urinary bladder, extending into the broad uterine ligament. Lateral to it are the internal iliac vessels and their branches and tributaries, the levator ani, coccygeus and obturator internus. Posterior are the sacral and coccygeal plexuses and above are the superior vesical and obliterated umbilical arteries. The plexuses contain numerous small ganglia. Each is formed by a hypogastric nerve, conveying most of the sympathetic fibres of the plexus, the remaining few arriving via branches from the ganglia. Parasympathetic fibres are derived from pelvic splanchic nerves. Preganglionic efferent sympathetic fibres originate in the lower three thoracic and upper two lumbar spinal segments, some relaying in ganglia of the lumbar and sacral parts of the sympathetic trunk, others synapsing in the lower part of the aortic plexus and in the superior and inferior hypogastric plexuses. Preganglionic parasympathetic fibres originate in the second to fourth sacral spinal segments, reach the plexus in the pelvic splanchic nerves and synapse in it or in walls of viscera supplied by its branches. Numerous branches are distributed to the pelvic and some abdominal viscera, either directly or along their arteries.

Parasympathetic fibres ascend in the hypogastric plexuses or as separate filaments to reach the inferior mesenteric plexus by way of the aortic plexus. By this route the descending and sigmoid parts of the colon recieve parasympathetic innervation.

Middle rectal plexus
This is formed by fibres from the upper part of the inferior hypogastric plexus to the rectum passing directly or along the middle rectal artery. It connects above with the superior rectal plexus and extends below to the internal anal sphincter. The rectal and anal nerve supply is from:

The superior rectal plexus


the middle rectal plexus


the inferior rectal (haemorrhoidal) nerves, branches of the pudendal nerve.


The parasympathetic preganglionic fibres from the rectal plexuses synapse with postganglionic neurons in the well-developed myenteric plexus, while sympathetic afferents pass through it without interruption. Efferent sympathetic fibres in the rectal plexuses inhibit the explusive musculature and stimulate the sphincter. Pain impulses traverse the sympathetic and parasympathetic fibres but the parasympathetic afferent and efferent fibres are more active in normal defaecation. Inferior rectal nerves supply motor fibres to the striated external anal sphincter and sensory (somatic) fibres to the lower (ectodermal) part of the anal canal (p. 194).

Vesical plexus
Coming from the anterior part of the inferior hypogastric plexus, this comprises many filaments which pass along vesical arteries to the bladder. Branches supply the seminal vesicles and deferent ducts. Many small groups of neurons exist among the nerve fibres in the vesical muscular wall. Sympathetic preganglionic fibres in the plexus are from the lower two thoracic and upper two lumbar spinal segments, synapsing with neurons scattered in the superior and inferior hypogastric plexuses and vesical wall. The parasympathetic preganglionic efferent fibres come from the second to fourth sacral spinal segments and synapse near or in the vesical wall with postganglionic neurons which stimulate its detrusor muscle and inhibit its sphincter. Efferent sympathetic nerves are motor to the sphincter and inhibitor to the detrusor muscle; but some maintain that they are mainly vasomotor and that vesical filling and emptying are controlled by parasympathetic nerves.

Prostatic plexus
Continued from the lower part of the inferior hypogastric plexus, this is composed of large nerves entering the base and sides of the prostate and contains neurons. It supplies: the prostate, seminal vesicles, prostatic urethra, ejaculatory ducts, corpora cavernosa, corpus spongiosum, membranous and penile urethra and bulbo-urethral glands. The nerves to the corporea cavernosa form two sets, the greater and lesser cavernous nerves, arising from the front of the plexus to join branches from the pudendal nerve and then passing below the pubic arch. The precise localization of the autonomic nerves from the pelvic plexus to the corpora cavernosa has been described by Lepor et al (1985) in the adult male pelvis. Lesser cavernous nerves pierce the fibrous penile sheath proximally to supply the erectile tissue of the corpus spongiosum and penile urethra. Greater cavernous nerves proceed on the dorsum penis, connect with the dorsal nerve and supply the erectile tissue, some filaments reaching the erectile tissue of the corpus spongiosum. Sympathetic supplies to the male genital organs produce vasoconstriction, the parasympathetic being vasodilator. Seminal vesicles are supplied from the vesical and prostatic plexuses and inferior hypogastric nerves; extensions pass to the ejaculatory and deferent ducts. Contraction of the seminal vesicles and ejaculation are considered to be due to the sympathetic supply, which also inhibits the vesical musculature and stimulates the sphincter during ejaculation, preventing reflux into the bladder. Others have suggested that contraction of the seminal vesicles is under parasympathetic control (Matthews & Raisman 1969).

Uterovaginal plexus
Uterine nerves arise from the inferior hypogastric plexus, mainly the part in the broad ligament, the utrovaginal plexus, from which branches descend with the vaginal arteries, while others pass directly to the cervix uteri or ascend with or near uterine arteries in the broad ligament. Nerves to the cervix form a plexus in which are small paracervical ganglia, one ganglion sometimes being larger and termed the utrerine cervical ganglion. Nerves ascending with the uterine arteries supply the uterine body and tube, connecting with tubal nerves from the inferior hypogastric plexus and with the ovarian plexus. The uterine nerves ramify in the myometrium and endometrium, generally accompanying the vessels. Efferent preganglionic sympathetic fibres are from the last thoracic and first lumbar spinal segments; the sites of their postganglionic neurons are unknown.Preganglionic parasympathetic fibres arise in the second to fourth sacral segments and relay in the paracervical ganglia. Sympathetic activity may produce uterine contraction and vasoconstriction and parasympathetic activity may produce uterine inhibition and vasodilation, but these activities are complicated by hormonal control of uterine functions.

Vaginal nerves from the lower parts of the inferior hypogastric and uterovaginal plexuses follow the vaginal arteries to supply the vaginal walls, the erectile tissue of the vestibular bulbs and clitoris (canvernous nerves of the clitoris), the urethra and the greater vestibular glands. The nerves contain many parsympathetic fibres which are vasodilator to the erectile tissue.

That's all there is in this section from Gray's. There is a section on enterics which I'm omitting.

I'll slowly bring more here from Burnstock's books, etc. Plese feel free to add material or links you might find on autonomics to this thread.

[Diane]

My copy of The Integrative Action of the Autonomic Nervous System: Neurobiology of Homeostasis (http://www.amazon.com/Integrative-Action-Autonomic-Nervous-System/dp/0521845181) by Wilfred Jänig, arrived yesterday. It's nearly brand new, only published this past June. Also quite reasonable as textbooks go, well under $200.

Chapter 4 alone is worth the price. It is titled The Peripheral Sympathetic and Parasympathetic Pathways, and contains 8 "sub"chapters, listed here:

4.1 Sympathetic vasoconstrictor pathways
4.2 Sympathetic non-vasoconstrictor pathways innervating somatic tissues
4.3 Sympathetic non-vasoconstrictor neurons innervating pelvic viscera and colon
4.4 Other types of sympathetic neuron
4.5 Adrenal medulla
4.6 Sympathetic neurons innervating the immune tissue
4.7 Proportions of preganglionic neurons in major sympathetic nerves
4.8 Parasympathetic systems


I have only browsed so far, but already I'm liking this book more than the Burnstock series on the ANS.. Burnstock simply provided within the covers of each of his books a bunch of already published studies. As an editor he did no editing at all, just collecting and re-publishing. And each book in the series (about a dozen books) cost as least as much as this one.

Janig takes the time to actually sit and synthesize everything. He does not predigest it at all but puts it through his mental blender a bit first, at least. And he's very careful to keep his own speculations separate from what's "known", plus at the end he has a very comprehensive list of what is not yet known.

I think I can trust this book. And as a humble human primate social groomer I very much appreciate that he's done some of the mental map making for me. :thumbs_up

[Diane]

Here is a short excerpt from Jänig's book (http://www.amazon.com/Integrative-Action-Autonomic-Nervous-System/dp/0521845181), based on this article (http://www.somasimple.com/forums/showthread.php?p=28006#post28006):
Type 1 allostatic overload occurs when energy demand exceeds supply, resulting in activation of the emergency life history stage. This serves to direct the animal away from normal life history stages into a survival mode that decreases allostatic load and regains positive energy balance. The normal life cycle can be resumed when the perturbation passes. Type 2 allostatic overload begins when there is sufficient or even excess energy consumption accompanied by social conflict and other types of social dysfunction. The latter is the case in human society and certain situations affecting animals in captivity. In all cases, secretion of glucocorticosteroids and activity of other mediators of allostasis such as the autonomic nervous system, CNS neurotransmitters, and inflammatory cytokines wax and wane with allostatic load. If allostatic load is chronically high, then pathologies develop. Type 2 allostatic overload does not trigger an escape response, and can only be counteracted through learning and changes in the social structure.
Not the distinction made between types of allostatic load.
1. Type one is stress induced by forces supplied directly from the environment. The creature is fully capable of pressing back as a living organism - responding powerfully, integrally, with the fullest of uninhibited responses.
2. Type two is stress induced by an environment that includes not only a metaphoric "rock" but also a "hard place". The creature has to be politically wise - it can't just rush to meet adversity with all its might, or run from it, instead it has to consider the "cost/benefit" of its response, and respond in some manner that costs personally/physiologically but won't rock the social fabric.

As a human primate social groomer, I think one of the biggest services I can provide is (a) a safe place in which patients can experience their own interoception and subsequent autonomic correction; and (b) some exteroceptively provided manual input to get (a) started.

Much more about this book can be read here (http://www.somasimple.com/forums/showthread.php?t=3331).

[Raulan2]

Diane,
With all this vital wiring piercing the diaphgram I would be inclined to predict that the "green light" types delineated on Nick's mechanical peripheral NS deformation thread lately, who can't abdominally breath and whose spines seem so rigid would maybe be nonconsciously guarding/defending their sympathetic chains. I wonder if the postural restoration people have looked into sympathetic nervous system anatomy, reflected on it, allowed it to inform their thinking to any extent?

Yes, we have!!!
Gee what a surprise, This is the main topic of the postural respiration course. Yes we do consider and express mesurements in terms of mesoderm, but I have been trying to tell you all that we are considering the importance of respiration and its effects on "mesodermal posture (function)", but more importantly on the autonomic nervous system and how it influences all systems, including ganglia etc..

[Mary C]

Raulan2

I found your comment today as I was going through the old threads on ANS.

Some French posters keep mentioning Janig but never bring any quotes from his writings. Now I can see why he is so important. This is probably what was missing from the theory in Souchard's RPG. I have not found any mention of autonomics on the RP (Mezieres) site so far.

Mary