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? 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 Debakey^12,26 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. Just ONE! It's not even in Gray's! 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.

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..