Thoracic Outlet Syndrome

[Diane]

From p. 39, Chapter 5 of the tunnel syndrome book:

Thoracic Outlet Syndrome
Thoracic outlet syndrome (TOS) has been investigated extensively to help accurately diagnose, evaluate etiologies, and expediently treat patients presenting with vague symptoms. Compression of the brachial plexus, the subclavian artery, or the subclavian vein before their division and separation, occurs in the area known as the thoracic outlet.1 Upper-extremity dysfunction may result from upper-limb pain, paresthesias, vascular insufficiency, and motor dysfunction secondary to compression and can be described as TOS. Its clinical presentation varies depending on when and which neurovascular structures are compressed. The term was first used in 1956 by Peet et al.2 Careful review of the literature reveals descriptions of similar syndromes: the anterior scalene syndrome by Adson and Coffey in 1927,3 the costoclavicular syndrome by Falconer and Weddell in 1943,4 and the hyperabduction syndrome by Wright in 1945.5 The present standard is dependent not only on those authors noted in this chapter, but also on all those whose efforts have yielded this body of knowledge. For didactic reasons, this chapter will present the TOS in separate syndromes, as it has been described chronologically in medical literature.

The clinical diagnosis of TOS remains complex, requiring detailed history, physical examination, and careful selection of appropriate tests. The presence of secondary gain makes patient selection for surgery extremely important. Conservative treatment remains the mainstay of all care. Therefore, close work with a therapist is essential.68

The differential diagnosis includes cervical radiculpoathy, supraclavicular fossa pathology, trauma, tumors (especially lung), brachial neuritis, distal compressive neuropathies, and complex regional pain syndrome type I (reflex sympathetic dystrophy).66

ANTERIOR SCALENE SYNDROME
The brachial plexus and the subclavian artery can be compressed as they pass between the anterior and medial scalene muscles and the first rib. This compression yields a characteristic neurovascular syndrome, the anterior scalene syndrome.

ANATOMY
The three scalene muscles originate from the transverse processes of the cervical vertebrae and insert on the first and second ribs. The anterior and medial scalene muscles insert on their respective tubercles on the first rib, sandwiching the subclavian artery (Fig. 5.1). The posterior scalenus muscle is fixed to the second rib. A variable scalenus minimus muscle may exist and insert between the anterior and medial scalenus muscles. The scalene muscles elevate the first and second rib during inspiration. Unilateral contraction inclines the head to the side of action and turns the face to the opposite side. Bilateral contraction flexes the cervical spine. The anterior and medial scalene muscles form one side of the posterior scalene foramen, with the sternocliedomastoid muscle and the first rib forming the other sides. Bounded by the anterior scalene muscle, the first rib, and the medial scalene muscle, the posterior scalene foramen admits the brachial plexus and the subclavian artery to the costoclavicular space. The posterior scalene foramen can range from 0.4 to 3.5 cm in width.6 Doesn't that seem like an anatomical casino? :cool: Lucky people who get a space that's a bit wider rather than a bit narrower.

The subclavian artery arches over the first rib and traverses the sulcus formed by the scalene muscles and first rib. Ther brachial plexus is composed of nerve roots from C5 to C8 and T1. The plexus may also receive contributions from the C4 (prefixed) or the T2 (postfixed) roots. It innervates the entire upper extremity and lies tautly stretched between the neck and shoulder without bony protection in this region.

Neurovascular compression can occur when disease or anatomical variations narrow this tight foramen. In the development of the anterior scalenus syndrome, anatomical variations are very important.7 They are described below.

ETIOLOGY
Naffziger and Grant11 and Oschsner, Gage, and Debakey12,26 have published cases where the anterior scalenus muscle alone, without the extistence of the cervical rib, is responsible for the compression of the neurovascular bundle with corresponding clinical symptoms. Komar13 summarized literature reviews of anterior scalenus syndrome. The anterior scalene syndrome has many similarities to the costoclavicular syndrome, also known as the syndrome of the cervical rib, described by Wilshilre8 in 1860 and Gruber9 in 1869.

Normal anatomy provides enough room in the posterior scalene foramen for the brachial plexus and the subclavian artery. However, many anatomical variations and dynamic changes in the anatomy can cause narrowing, lowering the threshold for development of clinical symptoms.14 Lord and Rosati9 stress the many embryological, anatomical, and physiological factors that create a disposition for compression.

The insertions of the anterior and medial scalene muscles on the first rib may approach each other, thereby narrowing the sulcus. Fibrous bands may connect the anterior and posterior scalene muscles, producing a sling that elevates the brachial plexus and the subclavian artery over the first rib.9 Some authors believe that even an unusually strong contraction of the anterior scalene muscle can profoundly elevate the first rib, further narrowing the foramen; however, in a series of hundreds of patients, despite sectioning of the anterior scalene muscle, Telford and Mottershead27 found the first rib to still be a problem. Sounds like they found out that you can't fight mesoderm with mesoderm.

The roots of the brachial plexus and the subclavian artery are bent under tension over the first rib, due to the change in posture from that of a quadruped to an erect person.15 A quadruped's thorax has its largest diameter in the anterior posterior dimension. A person's thorax has its largest diameter in the laterolateral dimension. The asymmetry of the thorax places a human's nerves and arteries in a position of tension.16 Poor posture, prolonged work above one's head, prolonged wearing of a knapsack, or advanced age can produce a lowered or anteriorly rotated shoulder and further increase the distance the nerves and vessels must travel.17-21 In adult women, the shoulder has a lower position in relation to the thorax than in men. Carrying heavy burdens on one's arms produces cervicobrachial traction that, when combined with increased respiratory exertion caused by work, results in high degrees of tension through the scalene foramen. Asymmetry of the foramen contributes to the unfavorable situation. The presence of a cervical rib or scalenus minimus muscle plays a role by either raising the floor of the foramen or narrowing the foramen in the anteroposterior dimension. The importance of scalenus muscle hypertrophy in narrowing of the foramen has been noted by Swank and Siomeone22 and Frankel and Hirata.23 Chronic vibratory trauma has also been implicated.24,25 Nerves hate vibration.

The vascular symptoms in the anterior scalene syndrome are caused by tension of the artery or vein over the first rib.28,29 Distal to the area of arterial compression or occlusion, one may find a post-stenotic dilatation. Vegetative nerve fibres are compressed at the same time as the neurovascular bundle.24,25 These can produce the vague nerve complaints.

CLINICAL SYMPTOMS AND SIGNS
The neurovascular symptomology depends on the frequency, duration, and degree of compression of the subclavian artery and the brachial plexus because of their location in the plexus. According to Komar,13 the symptoms can be arranged by their causes into four groups:
1. Neurological dysfunction
2. Vascular compression
3. Different body postures
4. Functional and anatomical changes of the scalene foramen

The lower roots of the brachial plexus (C8-T1) are at higher risk of compression than the higher roots. The symptoms generally include: pain in the fingers, hand, forearm, arm, and even the shouder; paresthesias, dysthesias, or hyperesthesia (the C8-T1 dermatomes). Numbness appears more often in the fingers, hand and forearm. More on this coming. It's a long chapter.

[Diane]

CLINICAL SYMPTOMS AND SIGNS (anterior scalene syndrome cont.)
Depending on the degree of arterial compression, ischemic signs of numbness, cold, weakness and skin color changes appear. Gangrene and ulcerations of the fingers may develop in severe cases. Ischemic pain can resemble pain from nerve compression. Weakened grip and impaired finger function could be present.

Neurological symptoms corresponding to the compression of the inferior part of the brachial plexus (C8-T1) result in paresis and atrophy of the hypothenar and interossei muscles. Vascular symptoms are manifested as intermittent ischemic crises similar to Raynaud's phenomenon. Primary Raynaud's phenomenon can coexist with thoracic outlet syndrome.31 Distal to the site of arterial compression can lie an aneurysm where thrombi may develop. Freed emboli can obliterate one of the terminal finger arteries, which is followed by severe pain.

Adson's sign represets a diagnostic test to elicit symptoms based on body posture.32,33 The sign utilizes movements that stretch the anterior and medial scalene muscles and potentiate any neurovascular compression in the region of the first rib. The examiner evaluates the strength of the radial pulse in the hanging arm as the patient inspires deeply, extends the neck, and turns the head in both directions. Without prompting, a patient should indicate reproduction of symptoms. Since the pulse may weaken or disappear in normal subjects,34 one must also examine other signs and perform other tests such as arteriography before proceeding to surgery. Arteriography, ultrasound, or auscultation might allow detection of subclavian artery compression during an Adson's test. With a return to normal posture, the pulse of a normal person with a positive Adson's test will return much quicker than that of a person with anterior scalene syndrome.13

French investigators describe an additional test, the signe des plateaux. The arm is abducted and placed parallel to the ground with the palm up. The radial pulse disappears when resistance is applied to the arm. When the patient's arm is supported in this position the pulse remains. Rather than depend on palpation, oscillography can be used. The presence of a cervical rib may be seen on plain radiographs. The relative value of electrophysiological studies in so-called neurogenic TOS has been stressed by many authors,35-38 but remains uncertain.65,66 Hypertrophied and taut anterior scalenus muscles and cervical ribs can be palpated in the supraclavicular region. While more than one test is available, none is absolute, thus initial conservative therapy remains mandatory. Treatment suggestion from the book include sensible things like minimizing the loads carried on shoulders from bags etc., ergonomics at work, better bras, breast reduction, better pillows.. Suggested PT is (as always in this book) to strengthen that which is perceived to be weak, against all reason, and ultrasound to anything perceived to be too tight. Surgical options include scalenectomy and rib resection, removal of the perceived offending mesoderm in other words.

Now we move to another perceived type or subcategory of TOS:
COSTOCLAVICULAR SYNDROME
Costoclavicular syndrome occurs with compression of the subclavian artery, subclavian vein, and brachial plexus as they pass between the clavicle and the first rib. Falconer and Weddell4 describe this syndrome as separate from anterior scalene syndrome because of the vascular involvement.

ANATOMY
The costoclavicular space, triangular in shape, connects the cervical spine with the upper extremity; therefore, it bears the name canalis cervicoaxillaris. The boundaries of this space are as follows: anteriorly, the medial third of the clavicle and the subclavius muscle; posterolaterally, the upper margin of the scapula; and posteromedially, the anterior third of the first rib and the insertions of the anterior and medial scalene muscles (Fig. 5.2). The neurovascular bundle runs in the medial angle of this triangle. The subclavian vein lies medially in front of the anterior scalene muscle's insertion on the first rib and deep to the costoclavicular ligament and thickening of the clavipectoral fascia. The fascia extends from the coracoid process to the first rib (costocoracoid ligament). The subclavian arery briefly enters this space via the posterior scalene foramen to lie lateral to the subclavian vein. Passing between the anterior and medial scalenus muscles, the brachial plexus joins the vascular bundle in the costoclavicular space.

ETIOLOGY
When the costoclavicular space becomes narrowed by disease or dynamic compression, the neuromuscular structures are compromised.44-46 Roos and Owens47 described congenital anomalies associated with TOS. Abnormal anatomy such as congenital fibrous bands in the thoracic outlet predispose an individual for TOS following stress or injury.48 Functional or dynamic anatomy predominates as an etiology for clinical disease.49 The space may be narrowed by the following: arm elevation that rotates the clavicle posteriorly; deep inhalation that raises the first rib into the space, because the clavicle does not rise with inspiration; and trauma to the clavicle, first rib, or retrosternal dislocation of the clavicle.50,51 Leffert notes that muscle weakness (especially trapezius weakness), depression, obesity, and excessively large breasts can aggravate the symptoms.66 Although Pollack found cervical ribs in up to 1% of the population (50% bilateral) the presence of a rib does not confirm the diagnosis.

CLINICAL SYMPTOMS AND SIGNS
Patients with costoclavicular syndrome present with subjective complaints similar to those from patients with anterior scalenus syndrome. While the neurological complaints of pain, paresthesia, and hyperesthesia dominate in the anterior scalenus syndrome, vascular symptoms dominate in the costoclavicular syndrome.52 Vein compression leads to temporary or permanent edema. The radial arery pulse is elevated when the patient thrusts his chest forward and pulls the shoulders posteriorly and interiorly. (Note: there are many small typos in this book; I'm not sure if this is really supposed to be "interiorly." The author may have meant to say "inferiorly." When the errors are mere punctuation or obvious spelling I just correct them as I go. But this seems less clear.)Typically, the pulse weakens or diappears. Measurement using an oscilloscope can verify these changes; however, pulse dampening can occur in controls.53 Komar13 recommended arteriography to evaluate the changes in flow between positions. Venography and venous pressure measurments may aid in evaluation. Ultrasonography, computed tomography (CT), and magnetic resonance imaging54 are also useful diagnostic tools. Not many treatment options are stated, just a trial of immobilization and if that doesn't work, surgery, although they make a point that surgeries aren't all that successful.

Next, hyperabduction syndrome.

[Diane]

HYPERABDUCTION SYNDROME
Repetitive or prolonged hyperabduction of the arm stretches the neurovascular bundle under the pectoralis minor tendon and the coracoid process. The resultant symptoms of neurovascular compression known as the hyperabduction syndrome was first described by Wright in 1945.5

ANATOMY
Leaving the costoclavicular space, the three cords of the brachial plexus, the subclavian artery, and the subclavian vein pass under the insertion of the pectoralis minor muscle on the coracoid process. As this neurovascular bundle enters the axillary fossa, the artery and vein become known as the axillary artery and axillary vein (Figs. 5.1 and 5.2). Abduction to 180 degrees stretches the neurovascular bundle around a fulcrum consisting of the pectoralis minor tendon, the coracoid process, and the humoral head. The bundle may reach a 90º angle. The neurovascular bundle remains fixed, allowing relatively no motion. The bundle can compensate only by stretching, producing an increased tension along its components. Abduction of the arm narrows by producing 30º of elevation and 35º of posterior displacement of the clavicle, thereby narrowing the costoclavicular tunnel. The tunnel's anterior wall, consisting also of the pectoralis minor muscle, the subclavius muscle, and the costoclavicular ligament (the thickening of the clavipectoral fascia), is stretched and further brought posteriorly, pushing the neurovascular bundle against the fulcrum.

ETIOLOGY
Wright5 describes two critical anatomical points where compression of the neurovascular bundle might occur with the arm in hyperabduction: the first, while passing through the costoclavicular tunnel on slit; and the second, while passing under the pectoralis minor tendon at its insertion on the coracoid process. During abduction of the arm, the fixed neurovascular bundle can be compressed by the pectoralis minor tendon as well as by the humoral head.60 The characteristic position for testing is described as 180 degrees of shoulder abduction and elbow flexion. This test reproduces common sleep positions or functional positions of electricians, painters, bricklayers or masons. Spinner et al.61 describe a new cause of ulnar nerve compression by the chondropitrochlearis muscle, arising from the pectoralis muscle and crossing over the neurovascular bundle in the axilla. (OK. I have got to stop here and ask if anyone else ever heard of such a muscle? I could find only ONE! google reference (http://www3.interscience.wiley.com/cgi-bin/abstract/110499827/ABSTRACT#search=%22chondropitrochlearis%22). Just ONE! It's not even in Gray's! :eek: How often does one get stopped in one's tracks with the mention of something in the body one has literally never heard of before? Wow..) CLINICAL SYMPTOMS AND SIGNS
Pain, paresthesia, and numbness develop first in the fingers and later in the hand, In some patients, transitory ischemia and edema develop, resembling Raynaud's disease, which has been described by Beyer and Wright62 in 38% of patients with hyperabduction syndrome. Neurological deficits are usually absent. As paresthesias and pain develop, patients correct their arm position, limiting the duration of nerve compression.

If the arm is abducted to 90º and externally rotated in patients with hyperabduction syndrome, the subjective symptoms can increase, while the radial artery pulse may weaken or disappear. The sensitivity of this test, Wright's maneuver, can be increased by the patient's holding a deep breath.66 Additionally, further abduction (hyper-) can be added, However, similar to the anterior scalene syndrome or the costoclavicular syndrome, tests can be positive in normal patients. Additionally, while the Adson's test may be positive, Youman and Smiley63 described the occurrence of TOS with negative Adson's and hyperabduction maneuvers. Strauer and Rastan64 proposed venography, arteriography, and intra-arterial pressure measurments to accurately assess positional variations in any arm's vascular status. The overhead test is positive when patients hold their arms at full elevation (180 degrees) and open and close their hands repetitively. Symptom reproduction (cramping, fatigue, numbness) within 30 seconds is significant.66 Treatment includes avoiding hyperabduction and sectioning pec minor. Good grief. When your tests are inconclusively positive or negative you can always try cutting on some mesoderm I guess..

[Raulan2]

Diane,

This is why respiration is so important in my practice. I see 5-6 cases of this each week, at least. It is my contention that an abnormally shaped and therefore improperly leveraged diaphragm cannot meet the oxygen demands of the individual. This will necessitate the nervous system to engage the scalenes to help meet the O2 demands. They present as hypertonic, and in dysynchrony. I cannot think of a more gruesome surgery than a rib removal. In my experince correction of breathing, this would include improving rib cage kinematics and position (this is what I consider postural restoration), proper timing and sequenicng of breathing to allow them to restore their ability to breath autonomically without compensation, will reduce vasuclar and neuro compression

[Diane]

I agree that rib surgery sounds gruesome.

Do you do anything to treat the neck first? (by "neck" I mean everything you can get your hands on from (geographical as opposed to mesodermal) head to clavicles to shoulders.)
Do you clear the brachial plexus as best you can so that the brain doesn't feel obliged to get in the habit of guarding it during breathing?

[Raulan2]

Diane,

Yes, I may describe it from a mesodermal reference, and observation of breathing, palpation of neck muscles to determine tone. If a persons' position is patterned so that they have sub-optimal kinematics of the rib cage then I will employ manual or non-manual techniques to improve rib cage kinematics. Typically once this is accomplished there is a reduction in tone throughout the neck, because if the neck/head is level to the horizon, and the trunk(rib cage, mediastinum) is not, my preference and successes have been to restore "posture" (which in my mind is synonymous with "breathing") of the trunk first before attempting some technique for the neck, or telling my patients to sit up straight. I want them to be able to function with any movement without restriction. I may also consider manual release techniques for the pec minor, subclavius to "clear the brachial plexus". i dont use that term but by taking the neuro demand off of the scalenes it has been my experience that this will "clear the brachial plexus"

I really am gearing all of my treatment to the nervous system, and measuring it as it is expressed through the mesoderm. I think we are similar in that. That is why I am still here. I appreciate the direction you all are trying to move the profession away from a predominate " mesodermal" or orthopedic (gag me) model. after several months of this self analysis, and understanding the predominate views here, I think I have identified the key theoretical glitch.
It is my experience, and the experience of other professionals that I work with, i.e. a Neurologist who does not come from a mesodermal background, that there are strong neuromuscular patterns developed in the body. We both had observed these same patterns and had been questioning this prior to meeting each other. It has been our attempt to understand these patterns. I disagree with Barrett (and feel that there is contradictory and inconclusive research on both sides of the argument) that we are this organism of random unpredictable events. I pose these questions to myself: Why do we have 18-27 "pain points" with fibromyalgia, depending on authors, why do we have such specific "trigger points" sach as described by Travell? Can ideomotor movement correct ideopathic scoliosis?

What I am saying is that I don't disagree with your views that the nervous system drives all. But in my experience if that is patterned for long enough then the mesoderm will respond with changes that make the nervous system alter neural drive. I regard this as compensation, I think others call this adaptive potential, but I cringe at that term if it leads to tissue pathology.

Thanks for the conversation, I am leraning from you and I appreciate that.

[Barrett Dorko]

Raulan,

Compensation and Adaptive Potential are completely different things. I would refer you to my course manual, page 8.

Who ever suggested that ideomotion could alter the bony consequences of scoliosis, ideopathic or not? Please, tell me and I'll have a word with them.

Years ago I personally heard Dr. Muhammad Yunas, one of fibromyalgia's greatest researchers, say that the tender points supposedly present in this condition had been discredited and were no longer used by diagnosticians in his specialty.

Travell's trigger points have not to my knowledge been objectified or validated. It's a story many wish were true.

[Diane]

Roulan, I found this a very helpful essay to read, when I was trying to wean off mesodermal constructs myself.
REFERRED PAIN OF PERIPHERAL NERVE ORIGIN: AN ALTERNATIVE TO THE "MYOFASCIAL PAIN" CONSTRUCT (http://websites.golden-orb.com/pain-education/100137.php).

I appreciate what you explained in your post above. Hang in there. It's a collective learning experience for everyone. Keep Barrett in your field of vision.. without staring at him too hard..(;) ) He hasn't steered anyone wrong so far. Despite his comments about how no one "gets" him/his teaching, I think a few people do. Learning to think for yourself is the main message, and in the process it means taking on quite a bit of deconstruction work, which sucks, but there's no way round it. Better than the alternative which is to stay stuck with concepts that date back to 1900 or thereabouts.:thumbs_do

[Raulan2]

Barrett,

No one here has mentioned scoliosis. In taking the concepts that have been promoted here that the ectoderm controls all. Then ideopathic scoliosis is in essence a ectodermal issue. Current research and theory do support that this is a neurally driven issue , and the bony changes are secondary and develop over time, vs. being the sole source of the problem. Then I want to know if it has been your experience or theroetical belief that idomotor activity could altar the process? 98% of thoracic curves are to the right(Song, KS April 1993, p. 63, Journal of Musculoskeletal Medicine). This is true for C- curves, s-curves, and double-s curves. This suggests to me clear neuromuscular patterns, and not random chaotic events.

Diane,

thanks for the article I have read similar articles, and my thinking has been leading in that direction for some time regarding referrend peripheral nerve pain. In my experience I see patterns of pain regardless of its source. So my quest has been to understand what function has lead so many patients to present with similar problems. Sorry, I got so off track on this thread, I did not mean to hijack it, just my bizarre train of thought.

Barrett,
I hope you are not tiring of me yet, actually I know you are, but I know that your are passionate enought to put up with me for awhile yet.

raulan

[Barrett Dorko]

In taking the concepts that have been promoted here that the ectoderm controls all. Then ideopathic scoliosis is in essence a ectodermal issue.

I have no idea how you reached this conclusion. No one else here has, and it strikes me as simply untrue. Maybe you should try some other example. All we've said is that a great deal of chronic pain that spreads and is altered with movement can be explained by looking at the nervous system.

I presume that the origins of idiopathic scoliosis remain as mysterious as ever and, again, no one here has suggested that we assume that this is a problem born in the ectoderm or resolved with instinctive active movement. I hope you're not telling others that we apparently believe such things.

[Diane]

Roulan, idiopathic scoliosis is mostly an unfoldment problem (i.e. embryological) of the sclerotomes. This can affect everything from shape of vertebrae, to arrangement or length of the epaxial musculature that controls them, growing asymmetrically from a developmental/genetic control. It doesn't show up usually until adolescence, but that doesn't mean it wasn't there all along, waiting to flower in all its glory, just like puberty.

[Diane]

Here are some pictures of the brachial plexus:

[Diane]

Here are some more:

[Diane]

I included views of some nerves further along. Studying these pictures, I was struck by how interconnected the nerves are, anastomosing with each other and even with lateral curtaneous branches from the thoracics, wrapping around huge vessels, poking through muscles. No wonder they get pinched sometimes.
The first picture in post #12 shows the relationship between the brachial plexus and scalenes.

[kongen]

I've been thinking about the scalenes a little lately, considering that their referral pattern in the traditional trigger point charts is so vast, and gently poking them seems to create widely distributed pain, particulary posterior thoracic pain.
I can see them become hypertonic due to dysfunctional breathing patterns, but what other reasons can there be? From a protection point of view, what benefit to which tissue would the brain achieve from contracting the scalenes? Any ideas to get me going..

[Barrett Dorko]

Perhaps the brain wants them to contract as part of a motion designed to reduce acquired mechanical deformation in the nervous tissue. If this were the the case and the action was then restricted by another brain center for a variety of reasons, you'd end up with the scalenes in a persistent isometric state.

The only way to solve this problem, I assume, is to allow the muscle (the brain) to have its way.

[nari]

PTs for years have had concerns about the 'elevated shoulder syndrome' where pain is perceived in that region along with elevated shoulders for ease of discomfort. Normal or depressed shoulder girdles can stress out the plexus, so active retraction of the scapulae and shoulder depression can actually create more pain. Controlled breathing helps to reduce the pain of postural "correction".

All that is happening here, is an attempt by the brain to reduce tension in the brachial plexus and its branches, by contraction of the musculature.
The cycle can be interrupted by attention to the nervous system (by various means as described in this site) and the muscles will become isotonic.

That's been my logic for some years, anyway.

Nari

[Diane]

I agree with the thoughts expressed by Barrett and Nari .. think of the important vasculature and other tubing in the neck. I suspect the brain/scalenes try to protect all of it and the brain ends up pinching its own brachial plexus as a small price to pay for having patent carotids, or whatever..

I'd treat the superficial cervical plexus with skin stretch first, then teach ideomotor after. But that's just me.

[Julie]

Roulan, I found this a very helpful essay to read, when I was trying to wean off mesodermal constructs myself.
REFERRED PAIN OF PERIPHERAL NERVE ORIGIN: AN ALTERNATIVE TO THE "MYOFASCIAL PAIN" CONSTRUCT (http://websites.golden-orb.com/pain-education/100137.php).



Is this link working for others? Doesn't seem to work for me....

[Diane]

Here is the current link (http://www.pain-education.com/100137.php) to that article julie - sorry.

[Julie]

Thanks Diane!

For what it's worth, though it has been a while since I've read his texts, David Simons MD, who has spent his entire life studying muscles and their function and dysfunction, has a very thorough hypothesis about the genesis of trigger points. He brings it down to the level of the neuromuscluar junction, and describes a reduction in oxygen, and alteration in acetylcholine release/uptake, Ca+ channel dysfunction, etc. He is by no means ignoring the nervous system in his studies and writings and hypotheses. Here is a slide presentation he did: http://ergonomics.osu.edu/pdfs/2003%20STAR%20Symposium/Simons%20Trigger.pdf
Check out slides 18 - 25 or so. I dunno... maybe this should be it's own thread? If a mod wants to move it, feel free.

[Diane]

Thanks for the slideshow peek. Does Simons remove the skin layer in order to twitch the muscle? I realize this question seems impertinent. I am not directing it to you, just to the air in general. Also, I would beg to differ that muscle comprises half the body. Maybe in Netter pictures, but not in a real body.

[Jon Newman]

Hi Julie,

On slide sixteen it is noted that "Good ergonomics prevents MTrPs"

The statement isn't referenced so I'm assuming it isn't a statement of fact.
Have you found this to be true?

[nari]

An impressive presentation, but, as well as Diane's question, I have doubts on his premise/s.
Could he explain how trigger points can disappear from their sites without doing anything to them, and not necessarily anywhere near the 'points'?
Without elongating any muscle involved with the palpated points? This can occur with DNM, and neural mobilisations.

Just curious.

Nari

[Luke Rickards]

Jon,

When I did my review, I didn't find any evidence that addressing the so-called 'contributing factors' to MTrP development prevents MPS or is helpful in treating it.

[kongen]

Having experienced muscle tension melt away after doing ideomotion, I find it hard to disagree with Barrett.

I agree with Nari that the elevated shoulder is a defense, not a defect. I would like to think of hypertonic scalenes to be a defense aswell, but as Diane pointed out, hypertonic scalenes would elevate the first rib, decrease the size of the intervertebral foramina and thereby pinch the brachial plexus? The brain might want to protect other structures like you mentioned Diane, but I still have difficulty picturing it.. Will ponder some more.

[Barrett Dorko]

Kongen,

You're right, disagreeing with me is hard.

I would like to know what Simon's would have to say about abnormal impulse generating sites. It's hard to get the trigger point crowd engaged in any sort of discussion though, as veterans here know.

I say, "If you're using heavy pressure manually you'll have to come up with your own rationale. I don't have one for you that can be defended." Almost without exception the trigger pointers/punchers/gougers/mashers/prickers/rubbers/icers/heaters will say, "It works."

That's when I lose interest.

[Julie]

yes, i certainly know that there are differences in paradigm here. but i posted the link primarily to show the overlap. i know that when PTs are treating TPs with conventional means, they are usually not thinking about what's happening at the synaptic level. but when you look to the source of most of what's known about muscle pain, you find david simons. i've met david on multiple occasions -- i know him. and i can tell you that he is a tireless, passionate investigator, and a true scientist. he absolutely demands that there be biologic explanations for his clinical hypotheses, as do those here. and he has participated in, reviewed, and directed untold numbers of studies to look precisely at those explanations. so i guess what i'm saying is.... when you take it to the source, so to speak, there may be more similarities between these two paradigms than you initially thought. that's all.

julie

[Barrett Dorko]

If he's tireless then he should join us here. Ask him.

[Julie]

Barrett,

I hate to speak for Simons, as I don't want to do him injustice. But he talks of the importance of lengthening sarcomeres in order to address abnormal electrical impulses at the neuromuscular junction.... to restore blood flow and end the localized "energy crisis." He definately discusses abnormal electrical impulses and has done lots of looking at EMGs at TPs. I agree with you that heavy pressure does not seem to be necessary. I have witnessed TPs resolve with positional release DNM or other gentle means. But I guess I'm thinking that that doesn't necessarily negate his whole hypothesis.... just changes the order of the chicken and egg, so to speak.

[Julie]

OK. I'll ask him.

[Diane]

Yes, please ask him julie, because I'd like to ask him what he does with the skin when he's treating. It doesn't seem that he takes it into account conceptually, so I wonder how he gets under it, physically and therapeutically.

Barrett, Almost without exception the trigger pointers/punchers/gougers/mashers/prickers/rubbers/icers/heaters will say, "It works."
You forgot to include stetchers/sprayers/IMS'ers/massagers/ appliers of sustained perpendicular pressure.

[Julie]

Barrett, Diane et al...

Are there one or two links or articles or pages I could point him to as a primer?

Julie

[Diane]

Yes, send him this thread, http://www.somasimple.com/forums/showthread.php?t=2838#post34991
and send him the index of the site, http://www.somasimple.com/forums . Tell him he'll meet with a lively group with whom he can exercise his scientific synapses. :angel:

[Jon Newman]

Luke has a paper published on the topic. It's posted somplace here at Soma. Maybe someone can find it and add that the list for Julie to pass along.

[Luke Rickards]

Jon,
I am fairly sure Dr Simons is aware of my paper.

[Luke Rickards]

Here (http://www.somasimple.com/forums/showthread.php?t=1166) it is.

[Julie]

Hmmmm... I am disinclined to invite Dr. Simons here by sending him a paper that dismisses all direct TP work as ineffective. Especially since I certainly do not have a corresponding paper that shows the terrific efficacy of ideomotion, or DNM, or neuromobs, etc. My reason for inviting him here would be to engage in a scholarly discussion about the genesis of chronic pain, TPs, and the central and peripheral nervous system. Not to alienate him totally from the get-go. If it's getting into the basic science of why what we do works, then I think he might be interested.

[Diane]

If it's getting into the basic science of why what we do works, then I think he might be interested. Well, all we can do is ask him and see what he wants to do.

[Jon Newman]

Hi Julie,

My reason for inviting him here would be to engage in a scholarly discussion...

I suggested Luke's paper exactly because it is sholarly. I think it would be fine starting point for a discussion. The discussion itself need not have anything to do with ideomotion, DNM, neurmobs, etc.

[nari]

Hi Julie,

If one has a working hypothesis and that person has a scholarly interest in science, he/she should invite folk to show that the hypothesis is wrong. That's the purpose of all scientifically-based work. If a hypothesis/premise cannot stand up to criticism, then it loses value and credibility.
It's not a question of efficacy of application. Most things we do will always work for some patients.
But if we say that treating mesodermal structures is the physiological result of manipulating muscle and joint (and I use manipulating in the broadest possible sense) then we have to show that nothing else could possibly react or respond to such procedures.

Do you agree? :)

Nari

[Julie]

Nari,
Yes, absolutely. I do agree. Which is largely why starting off a discussion with him about how TP techniques do not work seems to be leading it off in the wrong direction. Of course they work, sometimes, for some patients. Now, the WHY is the question worthy of discussion.

[Diane]

Of course they work, sometimes, for some patients. Now, the WHY is the question worthy of discussion. Um, could it maybe have something to do with exteroception and the brains' (not the brain's, the brains') perception and response to it? Would he be willing to consider that?

[Julie]

Um, could it maybe have something to do with exteroception and the brains' (not the brain's, the brains') perception and response to it? Would he be willing to consider that?

I certainly hope so!

[EricM]

Wow, it would be great if Dr. Simons would chose to discuss his theories here. I've invited a number of scholars to participate here in the past, with little success, so it would be a real coup to hook Simons in. :) However, before such a discussion disintegrates into a debate over which treatment (trigger pointers/punchers/gougers/mashers/prickers/rubbers/icers/heaters/stretchers/sprayers/IMS'ers/massagers/ appliers of sustained perpendicular pressure) should be used, I think all can agree that to varying degrees of efficacy, that they can all 'work.' Understanding 'why' this can be so is precisely what SomaSimple is all about, and what Cory made a brilliant effort to answer in his Unified Theory (http://www.somasimple.com/forums/showthread.php?t=2823) thread. Therefore a reasonable topic to discuss might be; given what we already know about why so many different treatments for "TrP's can work to reduce associated pain, what can we deduce about what a TrP actually is? And, is this deduction consistent with modern science? (If anyone can state that more clearly please have a go.)

[boneill]

I would be happy to personally invite David Simons to this forum. I expect to see him next month at the International Myopain Society, World Congress on Fibromyalgia and Myofascial Pain in Washington Dc. www.myopain.org (http://www.myopain.org) We would love to see some somasimple people there.I am moderating a session there and hope to invite a number of colleagues to this site to share, as I am learning a great deal. As you might surmise from the speaker list, this is a scientific meeting. At the 2003 meeting in Florida, David Butler gave a one day workshop as well as a key lecture.
David has always been first and foremost a scientiist. Although slowing down a bit at 84, he is still quite active and sharp from a scientific perspective. He is in the process of writing and editing a 3rd edition of the Trigger Point Manual.

Bryan

[Luke Rickards]

....... a paper that dismisses all direct TP work as ineffective.Julie, did you actually read it?

I am disinclined to invite Dr. Simons here by sending him a paper that dismisses all direct TP work as ineffective. I certainly do not have a corresponding paper that shows the terrific efficacy of ideomotion, or DNM, or neuromobs, etc.I think this shows a degree of misunderstanding. As I stated in my paper, there is insufficient evidence that trigger point therapies treat trigger points, although there is some evidence that a few treatments that attempt to treat trigger points can improve pain-related outcome measures. The difference is in the construct. In the case of ideomotor therapy, no one is saying pain is caused by a dysfunction of the ideomotor system, or in DNM that the pain is caused by a dysfunction of the skin or cutaneous sensory feedback. If you say a certain pain is due to a MTrP, then you have to show that it exists, reliably locate it, AND that a treatment effectively eliminates the entity at the same time as symptoms improve. I won't go into the former now, but the latter issue simply hasn't been addressed sufficiently in research literature on MTrPs; in fact, it has barely been attempted.

[Jon Newman]

For further reading see the literature and research sections

David G. Simons Academy (http://www.dgs.eu.com/en/)

[Julie]

Sorry all, I've been out of the loop for a bit.... off enjoying this AMAZING summer we are having with my kiddos. But I'm back.....

Bryan, if you'd like to invite David Simons in person, that would be great. I would love to have him come here and discuss what he knows about the neurology involved with TPs.... I think it might be substantial. I could certainly follow-up your invitation with an emailed one. Let me know how he responds, and if you'd like me to do so.

And I love the idea of having him do a formal interview here. He may actually be more interested in something like that than the more informal message boards.

By the way, I went to the Myopain conference in Portland OR in 2001. I found myself renting a car and driving all the way home to Michigan in a complete daze, as I left the conference early when the planes flew into the twin towers. It was such a surreal time.

Luke, touche.... I had only skimmed the article when I responded initially. Now I've read it, and concur. Sorry, and thanks for that.

Julie