Announcement

**emad** · 22-05-2006, 06:35 PM

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** · 22-05-2006, 07:51 PM

The autonomic nervous system in vertebral pain syndromes

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** · 22-05-2006, 11:26 PM

Musculoskeletal pain and concomitant features

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 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** · 23-05-2006, 03:07 AM

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 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** · 23-05-2006, 04:33 AM

The next speaker was Mustafa al'Absi 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** · 23-05-2006, 04:54 AM

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** · 23-05-2006, 05:56 AM

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** · 23-05-2006, 03:40 PM

THE POSSIBLE BASIS OF SOME CLINICAL FEATURES

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, which features a depiction overall.

**emad** · 23-05-2006, 05:47 PM

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** · 23-05-2006, 06:56 PM

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** · 23-05-2006, 07:26 PM

1. Dissemination and amplification of autonomic effects

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** · 23-05-2006, 07:58 PM

Here's one article 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 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** · 23-05-2006, 08:14 PM

Pictures

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.

Attached Files

**Jon Newman** · 24-05-2006, 01:41 AM

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.

Announcement

Autonomic state in pain and correction

Autonomic state in pain and correction

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