Autonomic state in pain and correction

[Diane]

Dissemination and amplification of autonomic effects (cont)

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]

1. Dissemination and amplification of autonomic effects (cont.)

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

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]

3. Musculoskeletal changes: lesions of trespass

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]

4. Autonomic nerve involvement in referred pain and other symptoms

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.. ..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]

Capsaicin

Ian's link. 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.”