Chapter | 10 |

Thoracic outlet syndromeSusan W Stralka

CHAPTER CONTENTS

Overview and history of thoracic outletsyndrome 141

Patho-anatomical causes of thoracic outletsyndrome 142

Functional causes of thoracic outletsyndrome (MediFocus Guide 2009) 142

Entrapment sites 143

Inter-scalene space triangle 143

Costo-clavicular space (Talu 2005) 143

Sub-pectoralis minor space 144

Aetiology of thoracic outlet syndrome 144

Clinical symptoms of thoracic outletsyndrome (Sanders et al 2008) 144

Neurological symptoms 145

Arterial symptoms 145

Venous symptoms 145

Sympathetic mediated pain in thoracicoutlet syndrome 145

Diagnosing thoracic outlet syndrome 146

Differential diagnosis of(Brantigan & Roos 2004) 146

Provocative test – used in diagnosis ofthoracic outlet syndrome 146

Imaging assessment of thoracic outletsyndrome 148

Clinical treatment and management ofthoracic outlet syndrome 148

Therapy evaluation of thoracicoutlet syndrome 148

Breathing patterns 148

Muscle imbalance 149

Joint stiffness 149

Neurogenic pain 149

Intervention for thoracic outlet syndrome 150

Conclusion 150

OVERVIEW AND HISTORY OFTHORACIC OUTLET SYNDROME

Thoracic outlet syndrome (TOS) is a broad term used todescribe upper extremity symptoms. These symptoms arerelated to compression or tension of the brachial plexus, thesub-clavian artery and vein in an area located above the firstrib and behind the clavicle. Often, one patient may be seenby numerous specialists before this syndrome is identified.The anterior scalene muscle, the middle scalene muscle andthe first rib, border the thoracic outlet. Pathological or dys-function related to these structures aswell as the clavicle bone,pectoralis minor, omohyoid, subclavius, scalene minimus,cervical rib or transverse process of C7 have been associatedwith TOS (Mackinnon 1996). These neurovascular structuresin their course from the inter-scalene triangle to the axilla arecovered with a fascial sheath that is part of the deep cervicalfascia,which canbecomeproblematic (Atasoy 2004). Fibrousbands, both congenital and acquired, also restrictmovementsof the clavicle and first rib. The term TOS does not specify thecompressing agent and does not identify the structure beingcompressed. This syndrome should be differentiated by usingthe term arterial TOS (ATOS), venous TOS (VTOS) or neuro-genic TOS (NTOS).

Peet first used the term thoracic outlet syndrome in1956 and indicated that compression of neurovascular

141© 2011 Elsevier Ltd.

DOI: 10.1016/B978-0-7020-3528-9.00010-8

structures occur in the inter-scalene triangle causingcervical-brachial pain, numbness and other disorders ofthe upper extremity. He used this term to group themunder only one name representing a single common ele-ment of neurovascular structures (Samarasam et al2004). It was not until 1958, that Robb proposed theterm thoracic outlet compression syndrome. The clinicalsigns are variable due to the variety of tissue that can beinvolved as well as the compression or entrapment area(Fig 10.1). Today TOS is classified into three sections: bra-chial plexopathy (NTOS) which occurs 90% or greater,the sub-clavian vein (VTOS) which occurs 6–7% and thesub-clavian artery (ATOS) at 3–4% (Sanders et al 2008).

Compression of the vascular system is easier to identifyand presents more urgently with arterial or venous throm-bosis than the symptoms with NTOS (Fugate et al 2009).The main controversy in patients with this syndrome(NTOS) relates to diagnosis. Neurological type complaintssuch as paraesthesia, numbness and pain must be basedon interpretation of the history, symptoms or clinicalexamination. These symptoms make the NTOS syndromesomewhat of an enigma as some healthcare professionalstend to overdiagnose it and others underdiagnose it withor without correlating the clinical signs and symptoms.

PATHO-ANATOMICAL CAUSESOF THORACIC OUTLET SYNDROME

The thoracic outlet region includes three major areas inwhich compression can occur: inter-scalene space or trian-gle, costo-clavicular space, and sub-pectoralis minorspace. Other causes are congenital bony structures, fibro-muscular anomalies, postural deviations and muscleimbalances. It has been reported that subjects who havecongenital bony or fibro-muscular variations in the

thoracic outlet region and experience some type of traumaare at risk to develop TOS. Trauma can result in musclespasm, inflammation and fibrosis, which further narrowsthe spaces and results in compression of the neurovascu-lar structure (Atasoy 2004).

The incidence of a cervical rib is less than 1% and maybe bilateral. The cervical rib size varies from a bony exosto-sis to a full grown cervical rib with ligamentous cartilagi-nous or bony attachment to the first rib. The female:male ratio is 2:1 (Atasoy 2004). A cervical rib or other ribanomalies cause the brachial plexus to be pulled againstthe fascial bands and C8–T1 symptoms can develop. A cer-vical rib, along with forward shoulders and poor posture,can cause pressure on the plexus and the vessels. Followinga fracture of the first rib, excess callous formation can occurcreating a narrow space leading to pressure on the brachialplexus and sub-clavian vessels.

Functional causes of thoracic outletsyndrome (MediFocus Guide 2009)

Poor posture, abnormal breathing patterns, cervical or tho-racic dysfunctions, muscle imbalances and shoulder pathol-ogies are commonly seen in TOS. Abnormal posture inwhich the head and shoulders are held in a forward positionalong with arm elevation greater than 90� may cause neuro-vascular consequences. Over time, shortening of variousneck musculatures may occur which, in turn, causes poste-rior shoulder girdle weakness. The longus and longissimuscervicis, upper and middle rhomboids and lower trapeziusbecome weakened. To compensate for the forward orienta-tionof the glenoid fossa of the humerus, the serratus anteriormuscle becomes shortened by abduction of the scapula. Thisscenario causes lengthening of the lower and middle trape-zius in supporting the scapula causing a mechanical disad-vantage and early fatigue. These alterations result in the

Scalene (anterior)

Coracoidprocess

of scapula

Insertion ofpectoralis minor

ScapulaManubriumof sternum(anterior)

2nd rib1st rib

C7

Scalene (medial)

Clavicle

Acromion

Head ofhumerus

Subclavian vein

Subclavian artery

Fig 10.1 Anatomy of the thoracicoutlet area.

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upper trapezius, rhomboids major and minor muscles,along with the levator scapulae having to function as acces-sory muscles to elevate the shoulder and arm.

The entire cycle continues to cause weakness in somemuscles and shortening of other muscles. Other func-tional causes, such as abduction over 110�, put tensionon the median nerve causing the ancillary artery to becompressed in the bicipital groove. In the axilla, compres-sion can be caused by a fibrous extension of the latissimusdorsi and pectoralis major muscle as they insert in thebicipital groove. With arm abduction or external rotation,the neurovascular bundle is compressed under the archproducing symptoms. There are histopathological changesthat occur to a nerve undergoing chronic compression,which takes place in TOS. A thorough history, compre-hensive physical examination and specific provocationtest can identify the structure causing compromise as wellas to help determine muscle weakness and tightness.

Entrapment sites

Inter-scalene space triangle

The neurovascular bundle which includes the brachialplexus trunks and sub-clavian vessels runs from thebase of the neck towards the axilla and the arm. Thefirst narrowing area is the most proximal and is namedinter-scalene triangle. This triangle is bordered by theanterior scalene muscle anteriorly, the middle scalenemuscle posteriorly, and inferiorly along with the base isthe medial surface of the first rib (Atasoy 2004) (Fig 10.2).

The scaleneminimusmuscle, which is found in only 30–50% of TOS cases, is located between the sub-clavian arteryand the T1 root of the brachial plexus which can be a sourceof compression. The anterior and middle scalene muscles

are respiratory muscles, which elevate the first rib as wellas slightly flex and rotate the neck. The insertion of thesemuscles in the first rib overlaps and causes a V formation.This overlapping creates a narrow space, which causes thesub-clavian artery and the brachial plexus to be in a highposition. It has been noted in some cases the middle sca-lenemuscle inserts along the full length of the first rib creat-ing a narrow space through which the neurovascularstructures must pass. When there is overlapping of the sca-lene muscle, there is also a prominent transverse processof the C7 process and the cervical rib. This has often beendescribed as a U or sling formation by these muscles. Thismay cause elevation and pressure from the structuresbelow. At the proximal portion of the triangle, the scalenemuscles may overlap which again causes a decrease in theopening thus causing pressure from the brachial plexusabove. It has been noted that at times a thick fibrous cover-age of the plexus extending from the scalene sheathe cancause adhesions and pressure on the plexus. The scalenemuscles can scar or hypertrophy with trauma or repetitivemotion that further contributes to compression. Someresearchers have found atrophy of type IImuscle fibres, pre-dominance of type I fibres and a 25% increase in connectivetissue in the scalene muscles (Sanders 1990) followinginjury.

Costo-clavicular space (Talu 2005)

The costo-clavicular space is a triangular area borderedanteriorly by the middle third of the clavicle, postero-medially by the first rib, and postero-laterally by theupper border of the scapula. The sub-clavian artery, veinand brachial plexus all pass through the costo-clavicularspace (see Fig 10.2). Compression of the brachial plexusand the sub-clavian artery and vein can occur as the result

Long TN

1st rib

Interscalenespace

Subpectoralminor space

Middle scalene muscle

Anterior scalene muscle

Phrenic nerve

Costoclavicularspace

Fig 10.2 Three potential spaces inthe thoracic outlet area that can beresponsible for TOS.

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of congenital abnormalities, trauma to the first rib or clav-icle, and structural changes in the sub-clavian muscle orthe costo-coracoid ligament.

Compression can occur if the clavicle or first rib is frac-tured following by a hematoma occurring at the fracturesite resulting in excessive scar tissue and callus build-up.As mentioned earlier, persons with forward shoulderswhich represents poor posture or a disabling illness, maydevelop narrowing of the costo-clavicular space, whichhas been shown to lead to TOS symptoms. With shoulderabduction, the scapula and coracoid move downwardwhich causes traction on the subclavius muscle andcosto-coracoid ligament adding additional pressure onthe neurovascular structures. The clavicle, during shoulderabduction, moves backward and upward 30–35� at thesternoclavicular joint, which may add narrowing to thecosto-clavicular space.

Sub-pectoralis minor space

The sub-pectoralis minor space is located just below thecoracoid process and under the pectoralis minor muscleinsertion to this process (see Fig. 10.2). The pectoralisminor runs from the 3rd to the 5th ribs over the thoraxand ends at coracoid process. This muscle is completelycovered by the pectoralis major muscle. Withshortening, the pectoralis minor can lead to a narrow-ing in the sub-pectoralis minor space increasing pres-sure on the blood vessels and brachial plexus. Thetight pectoralis minor muscle may also compressthe neurovascular structures during hyper-abduction.Wright termed this syndrome as hyper-abduction syn-drome which closes down the costo-clavicular space dueto the up and down motion of the clavicle (Beyer &Wright 1951).

AETIOLOGY OF THORACIC OUTLETSYNDROME

TOS is 3–4 times as frequent in women as in menbetween the ages of 20–50 years of age (Brismee et al2004). It is speculated that females have less developedmuscles, a greater tendency for drooping shoulders dueto additional breast tissue, a narrowed thoracic outletand an anatomical lower sternum all changing the anglebetween scalene muscles. This may be a reason femalesare more prone to develop this syndrome (Hursh &Thanki 1985). Another rationale, why females are moreprone to develop TOS, could be an increase in hormonesthat cause laxity thus resulting in superior subluxation ofthe first rib due to hormonal influence (Brismee et al2004) (Table 10.1). Common symptoms collected from17 reports are listed in Table 10.2 (Sanders & Haug1991).

CLINICAL SYMPTOMS OF THORACICOUTLET SYNDROME (SANDERS ET AL2008)

The term vascular TOS is non-specific and it does notimply neurogenic, arterial or venous compression, andnot address what structure is involved. Historically, symp-toms and physical findings are more specific. Patient typi-cally complains of pain in the sub-scapular, scapular,cervical, cervical thoracic regions and occipital headaches.Paraesthesia and numbness may be present in the entirehand region or parts of it. Often using the arms in an

Table 10.1 Conditions causing nerve trauma (modified

from Sanders & Haug 1991)

Aetiology %

Neck trauma 86

Rear end auto accident 32

Side or front end auto accident 24

Work injury, including RSI 22

Other neck trauma 8

Cervical or anomalous first rib 2

Unknown or spontaneous 12

100

Table 10.2 Symptoms from nerve irritation (modified from

Sanders & Haug 1991)

Symptoms %

Neck pain 92

Shoulder pain 70

Arm pain 80

Paraesthesia 95

All 5 fingers 46

Fingers 1–3 30

Fingers 4–5 14

No paraesthesia 10

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elevated position exacerbates the symptoms and com-plaints are a heavy, tired, aching sensation along withnumbness or paraesthesia.

Common clinical presentation of TOS includes:

• Numbness/tingling in ring and small finger but canencompass entire hand

• Paraesthesia occur at night and/or during dailyactivities

• Vague pain in the uninvolved extremity can occur inhand, elbow, shoulder and/or cervical spine

• Subjective complaints of hand/arm weakness,especially with arms raised overhead

• Subjective complaints of swelling in the absence oftrue swelling

• The common symptoms collected from 17 reports arelisted in Table 10.2.

Neurological symptoms

TOS symptoms may develop spontaneously or followinginjury in the neck and/or shoulder region. A list of condi-tions causing nerve trauma are found in Table 10.1.Basic concepts of TOS are a mechanical predisposition(Brantigan & Roos 2004). Symptoms are primarily neuro-logic structural anomalies causing the problem. Traumamay precipitate the neurologic type of TOS in certainsusceptible individuals. The upper plexus includes symp-toms involving the C5, C6 and C7 while the lower plexusprincipally involves the C8–T1 levels.

When the upper plexus is involved, there is pain in theside of the neck and this pain may radiate to the ear andface. Headaches are not uncommon when the upperplexus is involved. Some patients state that on the affectedside, there is a ‘stuffy ear’. Often the pain radiates from theear posteriorly to the rhomboids and anteriorly over theclavicle and pectoralis regions. The pain may move later-ally to the trapezius, deltoid muscle and down theC5–C6 radial nerve area. Lower plexus patients havesymptoms that present in the anterior or posterior shoul-der region radiating down the ulnar side of the forearminto the hand, the ring and small finger, as well as muscletenderness with trigger points which can be located in thesupra-clavicular and infra-clavicular area. Headaches maybe disabling and can increase with arm activity. At times,the pain with lower plexus involvement mimics the painassociated with cardiac angina.

Injury or repetitive stresses causing chronic musclespasm may precipitate the syndrome. A common problemis hyperextension-flexion or whiplash injury of the neck.The TOS symptom may show up immediately or may bedelayed for weeks or months. Usually cervical and shoul-der sprain symptoms occur immediately after the whip-lash with persisting symptoms of neck and shoulderpain and stiffness before being diagnosed as TOS(Brantigan & Roos 2004). As the whiplash symptoms

gradually improve over time, the post-traumatic TOSinvolving the brachial plexus worsens.

Arterial symptoms

Symptoms of ATOS usually develop spontaneously unre-lated to trauma or work. These patients often have trueclaudication of the arm particularly when the arm is ele-vated. These arterial symptoms occur from compressionof the sub-clavian artery in the area of the first rib. Arterialsymptoms differ from the whole arm numbness andheaviness that persists when the arm is elevated inpatients with neurologic TOS as well as presenting withvery little shoulder or neck symptoms. Patients with arte-rial symptoms may have a cervical rib or an enlargedtransverse process of C7 causing the problem.

Physical findings are those of arterial occlusion: loss ofpulses at rest, perhaps colour changes and ischemic fingertips as well as coldness, paraesthesia and fatigue. Arterialsymptoms include digital and hand ischemia symptoms(coldness, pallor, paraesthesia and fatigue of the arm).In the supra-clavicular area, there is sometimes a tenderlump, bony prominence or even pulsation of the sub-cla-vian artery. Arterial TOS accounts for less than 5% of TOSand typically results from long-term intermittent vascularcompression. A cervical x-ray is used as a screening testto rule out ATOS (Brantigan & Roos 2004).

Venous symptoms

The VTOS comprises 2–3% of all TOS patients. Venoussymptoms may be preceded by excessive activity with theupper extremity. The precipitating factor that leads tothrombosis is excessive activity of the arm such as throw-ing a baseball, swimming, weight lifting or working witharms elevated. Swelling, oedema, cyanosis and arm dis-comfort, which is aggravated with exercise along with dis-tended superficial veins, shoulder and chest wall, areresults of venous symptoms.

It is not uncommon tohave a sub-clavian vein thrombosisat the first rib level.When this occurs, there is a sudden onsetof dusky cyanosis, edema and extreme limb discomfort. It isimportant to diagnose this immediately and surgical decom-pression is necessary so that the symptoms do not becomechronic. Physicians who diagnose only the vascular formsof TOS are misdiagnosing the vast majority of patients whohave nonvascular TOS (Brantigan & Roos 2004).

SYMPATHETIC MEDIATED PAININ THORACIC OUTLET SYNDROME

Some of the painful symptoms in individuals with NTOSmay be due to overlapping signs and symptoms of com-plex regional pain syndrome (CRPS) (Kaymak & Ozcakar

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2004). In NTOS, the coldness and colour changes maynot be caused by ischemia due to obstruction of thesub-clavian vessels, but due to an overactive sympatheticnervous system (SNS). Allodynia, hyperalgesia, prolongedperiods of red or blue hand, persistent edema, excessivewarmth and sweating changes are often present.

Sympathetic mediated pain may be related to a directinjury to the sympathetic axons in the cords or trunks ofthe brachial plexus as well as an activation of thesomato-sympathetic reflex in which a somatic root injurywill activate the sympathetic system over several ascend-ing and descending dermatomes (Schwartzman 1987,Casey et al 2003). Anatomically, the SNS fibers run onthe circumference of the nerve root of C8, T1 and lowertrunk of the brachial plexus. When the nerves are com-pressed the sympathetic fibres are activated producingRaynaud’s phenomenon. This may explain how the cold-ness and colour changes are frequently seen with bothNTOS and ATOS.

Often, clinicians use the term compressor or releaser tocategorize symptoms. The term, compressor, is used toevaluate patients who complain of symptoms whenperforming overhead activities. These patients have notparaesthesia at night unless the arm is overhead andwhose occupation requires overhead work for long peri-ods. This compression occurs when the arm is raised over-head which then causes the brachial plexus to turn overthe first rib then under the clavicle at the costo-clavicularspace. When the patient lowers their arm, the compres-sion on the blood supply to the nerve is off and the symp-toms decrease.

Women often report release phenomenon more oftenthan men due to the weight of the breasts pulling ontheir bra straps and/or kyphotic posture. The bra strapsare capable of creating compression of the brachialplexus while the kyphotic posture in which there is anincrease of the shoulder girdle causes increased tensionof the brachial plexus and closes down the thoracic out-let. Brismee et al (2004) showed that women were foundto report symptoms associated with the release phenom-enon about twice as often as men. The Roos Test is oftenpositive when a patient has what is commonly calledcompressor TOS.

The term ‘releaser’ is used to identify patients that expe-rience symptoms primarily at night who work in moresedentary jobs and these patients may have poor posturealong with large or heavy upper extremities. The term‘release phenomenon’ means the brachial plexus is beingpulled down then venous pooling occurs around thenerve, which inhibits blood flow to the peripheral nerve.Gravity has an effect when sitting and standing whichplaces tension on the nerve. When the patient lies down,the tension is gradually released and the blood flowreturns to the nerves. As reported by Liu, it takes 4–6hours after the removal of compression for the blood flowto return to the nerve. This may explain why a patient

aches at the same time every night with paraesthesia orpain. Lundborg (1970) believes this happening at nightis due to the axons firing and patients experienceparaesthesia.

DIAGNOSING THORACIC OUTLETSYNDROME

The diagnosis of TOS is essentially based on history andclinical examination. In order to diagnose accurately,clinical presentation must be evaluated as either neuro-genic or vascular. Neurogenic is linked to compressionof the brachial plexus and vascular is compressionof the sub-clavian vessels. TOS manifestations are variedand there is no single definitive test. Common symptomsexperienced with TOS include paraesthesia, numbness,pain and burning. Advanced symptoms include muscleweakness especially in the ulnar nerve distribution.

Diagnosis is based on a total clinical picture that iscomprised of a careful meticulous history, review of med-ical records and clinical examination. For NTOS, theexamination also includes tenderness over the scalenemuscles, trapezius muscle and anterior chest wall, a posi-tive Tinel sign over the brachial plexus in the neck,reduced sensation to very light touch in the fingers anda positive response to several provocative manoeuvresthat put stress on the plexus to elicit symptoms. A list ofthese manoeuvres and incidence of positive responses isseen in the symptoms in Table 10.2.

Differential diagnosis (Brantigan &Roos 2004)

To have a precise diagnosis, it must be made by history,physical examination, provocative tests, and if needed,ultrasound, radiologic evaluation and/or electrodiagnosticevaluation (Brantigan & Roos 2004). There are multiplediagnoses to consider in the differential diagnosis ofTOS. Consideration must be given to musculoskeletalpathology that could mimic a TOS presentation. Cervicalradiculopathy as well as ulnar neuropathy may presentwith similar symptoms as TOS including hypothenarand/or intrinsic wasting (Box 10.1).

Provocative test – used in diagnosisof thoracic outlet syndrome

The physical examination as well as the other tests mustbe done as to not exacerbate the symptom. Clinicians relyon clinical tests for alteration of radial pulse. A few ofthese tests are listed below (For all tests, the patient is ina seated position and the examiner palpates the radialpulse):

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(A) Adson Test: The patient is asked to rotate the head andelevate his chin toward the affected side. If the radialpulse on that side is absent or decreased, the test ispositive showing that vascular component of theneurovascular bundle is compressed by the scaleneanterior muscle or cervical rib. This test has shown asensitivity of 79% and specificity of 76% (Gillard et al2001).

(B) Wright’s Test: The patient’s arm is hyper-abducted. Ifthere is a decrease or absence of a pulse on one side,the test is positive showing that the axillary artery iscompressed by the pectoralis minor muscle orcoracoid process due to stretching of theneurovascular bundle. Gillard et al (2001) found asensitivity of 70% and specificity of 53% for pulseabolition.

Patients with intermittent symptoms that are associatedwith specific movements or positions of the upper quad-rant, which increases or decreases the compression andtension of neuro structures, will need to utilize these testsbelow:

(A) Roos Test: the patient has arms at 90� abduction andthe therapist puts downward pressure on the scapulaas the patient opens and closes the fingers. If the TOSsymptoms are reproduced within 90 seconds, the testis positive.

(B) Cyriax Release Test: the patient can be sitting orstanding with arms supported or resting on a pillowwith forearm at neutral for a period of at least 3minutes since symptoms, such as paraesthesia and

numbness may not occur instantly. This positionpassively elevates the shoulder girdle bilaterally withthe patient’s trunk positioned posteriorly to assureshoulder girdle end range. A positive test is when arelease phenomenon occurs including reproductionof symptoms. One theory suggests that paraesthesia isthe most common symptom for those individualswith a release phenomenon followed by numbnessand occasionally, pain. According to Cyriax (1978),paraesthesia and numbness appear when a nerve trunkor cord is first compressed, followed by a return ofnormal sensation. After pressure is released from theplexus, these symptoms reoccur latently. This outcomeis different from the phenomenon associated withnerve root compression, which produces persistentsymptoms until the root pressure is released (Cyriax1978, Brismee et al 2004). Brismee et al (2004)showed that a one-minute modified Cyriax ReleaseTest is the optimal time limit to maximize thespecificity of the test (specificity of 97%).

(C) Costo-clavicular Test: This test may be used for bothneurological and vascular compromise. The patientbrings his shoulders posteriorly and hyper-flexes hischin. A decrease in symptomsmeans that the test ispositive and that the neurogenic component of theneurovascularbundle is compressed. This test has showna specificity ranging from 53% to 100% depending onthe assessment of vascular changes or pain, respectively(Ryan & Jensen 1995, Nord et al 2008).

(D) Elevated First Rib Test: For right first rib elevation,patients will demonstrate a significant loss of rightlateral flexion with hard end-fill in the position ofleft rotation indicating an elevated hypo-mobile firstrib on the involved side. The second phase of the testconsists of passively rotating the neck to thesymptomatic side (example: right) to end range thenfollowed by lateral flexion of the neck to the left. Thistest is considered positive when there is a decrease oflateral flexion and a hard end-fill on the effected sideas compared to the contralateral side.

(E) Upper Limb Neurodynamics Testing: This test is used torule out neurogenic pain and to provoke symptoms.Neural tissue assessment can be assessed by activemovement dysfunction, passive movementdysfunction, adverse response to neural tissueprovocation test, hyperalgesic response to palpationof nerve trunks, hyperalgesic responses to palpationof related cutaneous tissue and evidence of relatedlocal pathology (Hall & Elvey 1999). For this topicsee Chapter 38.

The study by Sanders et al (2008) reported on 50 patientswith positive provocative testing (Table 10.3). Gillard et al(2001) showed that a cluster of two provocative tests dis-played the highest sensitivity (90%), whereas a cluster offive provocative tests increased the specificity to 84%.

Box 10.1 Differential diagnosis of thoracic outletsyndrome (TOS)

• Cervical disc disease

• Cervical facet disease, spondylosis

• Malignancies (Pancoast tumour, local tumours; e.g.

nerve sheath tumours, spinal cord tumours)

• Peripheral nerve entrapments (ulnar and/or median

nerve entrapment)

• Brachial plexitis

• Shoulder pathology

• Muscular spasms, fibromyalgia

• Neurologic disorders (multiple sclerosis)

• Chest pain, angina

• Vasculitis

• Vasospastic disorder (Raynaud disease)

• Neuropathic syndromes of upper extremity (CRPS I, II)

• Thoracic 4 Syndrome (T4)

• Sympathetic mediated pain

• Dull pain, discomfort, aching with tightness in

mid-thoracic area

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Imaging assessment of thoracicoutlet syndrome

TOS presents a challenge to diagnosticians and controversyexists regarding what test and imaging assessment shouldbe used for diagnosis. Unfortunately, many physiciansdoubt the diagnosis of the pathology because it cannotbe radiographically or electro-physiologically determined.One school of thought suggests that patients must demon-strate true neurological signs to be diagnosed with TOS andbe confirmed by electromyography or nerve conductionvelocity for brachial plexus compression and/or Dopplerstudies for vascular compromise as well as radiography torule out cervical rib.

Another school of thought would diagnose TOS by theinterpretation of the history, symptoms and clinical examina-tion. Clinical testing of TOS has been highly debated in litera-ture andno single test or questionnaire is universally acceptedfor the diagnosis of TOS (Mackinnon & Novak 2002).

Clinical diagnosis can be assisted by the use of imagingto demonstrate the nature and location of the structureundergoing compression and the structure producingcompression but this is not always necessary. The firstradiographic procedure should be a cervical plain radiogra-phy to assess for bone abnormalities as well as to differenti-ate the diagnosis. Computed tomography and angiographyormagnetic resonance imaging (MRI) should be performedwith posturalmanoeuvres in order to dynamically show thecompression (Demondion et al 2006).

CLINICAL TREATMENT ANDMANAGEMENT OF THORACIC OUTLETSYNDROME

Conservative treatment is indicated in patients unlessthere is significant neural loss or vascular compromise

(Leffert 1991). The focus for conservative treatment is todecrease extrinsic pressure reducing intrinsic irritation.The goal is to decrease pressure on the neurovascular bun-dle and give the patient the tools to manage their TOS.Conservative management of TOS consists of (not inany particular order): restore normal breathing patterns,reduce inflammation, decrease muscle tension, elongatetight muscles, strengthen weak musculature, maintainneural excursion, maintain mobile joints, improve pos-ture and body mechanics, and to restore muscle balance(Watson et al 2009).

Therapy evaluation of thoracicoutlet syndrome

The subjective history examination is most helpful tounderstand patients’ perception of the symptoms andduration of time or chronicity of the symptoms. The diag-nosis and effective treatment of patients presenting withTOS is challenging due to a syndrome involving manypain sources. Provocation and specific functional testsprovide information to design an orthopedic manualtherapy management programme as well as addressingother dysfunctions. TOS can cause pain in the cervicaland thoracic area, in specific muscle groups and paraes-thesia and numbness in the upper extremity. It is impor-tant to identify the structure causing the symptoms andidentifying areas of hypo-mobility or hyper-mobility.The provocation tests are important to assist in isolatingthe pain generators and the mobility testing determinesareas of segmental dysfunction. It is this author’s experi-ence that identifying the abnormalities in the followingareas and designing a treatment programme around theseabnormalities will assist in successful outcomes.

Breathing patterns

Analysing the patient’s breathing pattern cannot beunderstated. Patients with TOS tend to breath with theirupper thorax without any abdominal movement. Whenthis occurs the accessory muscles, particularly the sca-lene, elevate the first rib thus causing narrowing ofthe thoracic outlet. When examining a patient whouses the accessory respiratory muscle, as opposed to dia-phragmatic breathing, it is not uncommon to find adecrease in hand temperature and decrease in bloodflow because of abnormal sympathetic tone or vascularcompromise. The sympathetic nervous system uses thisnormal protective response of vasal restriction thatalters blood flow. It is important to change the breath-ing pattern to a more relaxed diaphragmatic breathingthat allows for opening in the thoracic outlet andreduces muscle tension. The abnormal breathing patternof not using the diaphragm perpetuates a vicious cycleof pain, spasm and congestion. The key to teaching is

Table 10.3 Positive physical findings (modified from

Sanders et al 2008)

Positive physical findings – 50 patients %

Upper limb tension test (ULTT) 98

90� abduction in external rotation 100

Scalene muscle tenderness 94

Scalene pressure yields radiating symptoms 92

Neck rotation to opposite side 90

Head tilt to opposite side 90

Sensation to light touch 68

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to ask the patient to lie supine with both hands placedon the upper abdomen and lower rib cage. The abdo-men lifts with respiration and lowers with expiration.Observing hand movement will determine if breathingis done correctly. The scalene, in abnormal breathing,tends to contract through the full inspiratory phase.This maintains the elevation of the first rib, which inturn, will compromise the space for the sub-clavian veinto not be compressed.

By performing relaxed repeated breathing patterns,there is a decrease in muscle tension. Imbalances inthe pressure gradients with TOS cause an increase intunnel pressure causing venous stasis and hypoxia. Ifthis hypoxia continues the oedema around the nerveas well as fibroblastic changes can cause scarring. Edge-low (2004) uses an analogy to describe this situation asa river flowing into a lake and a river flowing out of thelake, in which the inflow equals the outflow. In thisstate, the volume of the lake is constant, the oxygencontent is high, and the pollution content is low.Should there be an obstruction affecting the outflow,then the volume of the lake would increase, the oxygencontent would decrease and the pollution wouldincrease

Muscle imbalance

Muscle imbalance is a major source of symptoms inpatients with TOS. Abnormal posture, such as forwardhead, rounded shoulders and protracted shoulders aredamaging posture for the scapular and neck musclesand should be addressed immediately. It is importantto make sure that the scalene muscles, which elevatethe first rib, are not tense. If the scapula muscles areweak, then an abnormal scapular movement pattern willresult in weakness in the middle and lower trapezius andserratus anterior muscles. The scalene can overwork thuscausing more entrapment. A posture evaluation shouldinclude evaluating multiple joint and scapula move-ments. It is important to assist the scapula position atrest and see if the scapula is depressed and downwardlyrotated which can be contributing factors to TOS. Withthe above example, the scapula would be lower thanT2–T7 and the slope of the shoulders would be increasedwhich would make the neck appear longer. With scapuladepression during overhead reaching, there are changesoccurring at the acromio-clavicular joint (AC) especiallywith large and heavy arms. The AC joint, usually at theend range, will show creases that increase in overheadactivities. Scapula, downwardly rotated, can be identifiedbecause the inferior angle of the scapula is closer to thespine than the superior angle. Another way to assess down-wardly scapula rotation is evaluating movement into flex-ion and abduction. This movement normally causes signsof pulling or pain located in the teres major and latissimusdorsi region (Sahrmann 2002).

Joint stiffness

The brachial plexus can be compressed with joint stiffnessor capsular tightness. Several authors have proposedmobilization of the cervical, thoracic, sternoclavicular,acromio-clavicular and costo-transverse joints to improvejoint stiffness or hypo-mobility, range of motion and cap-sular tightness in upper quadrant conditions (Brismeeet al 2005, Vanti et al 2007). Manual therapy techniquesaimed at the joints, soft tissue and neural structure ofthe upper quadrant including the cervical and thoracicspine have been successful in treatment. Research hasshown that thoracic mobilization, especially at the T4area, is helpful to provide an inhibitory influence on thesympathetic nervous system and causes immediate posttreatment pain relief (Yip-Menck et al 2000). Thoracicmobilization has proven effective in improving posture,hand and skin temperature as well as pain in TOS (seeChapter 11). The study by Stralka (2010), using grade IIIoscillation movement PA at T4 level, showed similaritiesin increased hand and skin temperature. Taskaynatan et al(2007) reported that inclusion of mechanical cervical trac-tion reduced complaints of numbness in patients with TOS.

Evidence exists that thoracic joint mobilizationdecreases pain (Colachis et al 1966, Saal et al 1966, Brow-der et al 2004) and it has been theorized that biomechan-ical disturbances of the thoracic spine can contribute tocervical disorders (Greenman 1996, Norlander et al1997, Browder et al 2004, Gross et al 2004). When thesympathetic nervous system (SNS) responds there is anormal protective response of vasoconstriction that altersblood flow. Automatic improper breathing patterns alongwith pain, stress and anxiety can cause SNS activity thatmaintains a cycle of pain, tension and dysfunction. Theinvolvement of SNS by researchers is controversial butmy experience has shown that by changing the sympa-thetic activity, there can be a positive influence on thepatients’ symptoms.

Neurogenic pain

It is the author’s experience that upper limb nerve tensiontesting provocative manoeuvres along with clinical exami-nation are extremely helpful in identifying NTOS. Neuralmobility is an important part of a successful outcome. Theprovocation testing will reveal if the patient is a releaser ora compressor and this is useful in educating the patient towhich positions of comfort will decrease symptoms. Thisupper limb nerve tension testing is useful to identify thearea of specific entrapments of the brachial plexus. WithTOS, the lower trunk/medial cord (C7–T1) is most com-monly involved. The upper limb nerve tension testing andTinels often locate the neurogenic irritability both proximaland distal, which is commonly referred to as a double crushsyndrome (Plewa & Delinger 1998). These tests should notaggravate the symptoms (see Chapter 38).

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Reproduction of radiating neurogenic arm pain withparaesthesia is a positive response. When this test is posi-tive, it is an indicator of compression against the nerveroots or brachial plexus.

Intervention for thoracic outletsyndrome

There are many schools of thought contributing to thetherapy management of TOS. Peter Edgelow, a phy-siotherapist, utilizes three concepts that are the guidingprinciples for effective treatment of neurovascular entrap-ment, which are built on the fundamental idea that thisentrapment occurs as a consequence of trauma affectingthe nerve or vascular system (Edgelow 2004). His firstconcept is patient empowerment, which means thepatient must be responsible and in control of his own carein order for treatment to be long lasting. The importanceof treating the whole person cannot be underestimatedand is supported by this author. The most successful out-comes are a multi-factorial approach starting with patientempowered to take care of their own problems by under-standing their TOS dilemma as well as understanding thetreatment solution. In treating, it is important to gain thepatient’s trust, stay in contact with them and make surethey understand their problem. The impact of having thislong pain syndrome without correctly being diagnosed asTOS allows individuals to feel their life is out of control.Restoring the feeling of being in control has a positiveimpact on the individual. It has been my experience thatthere is no quick fix in treating patients with thoracic out-let syndrome. That is why patients must understand thelength of the programme and being diligent with the exer-cise programmes. It is also important for the patient tounderstand the risks and rewards in paying close attentionto symptoms. By understanding the problem and thesolution, it adds control in the patient’s life. Edgelow alsosuggests that individual risk factors, health habits, dailyliving demands and belief systems that can be controlledare important for the treatment of TOS.

The second concept is that neurovascular entrapment is aproblem of stenosis. Stenosis should not be thought of as arigid narrowing of an anatomic part, rather a series of eventsand circumstances. These events may result in irreversiblenarrowing. The stenosis caused by the presence of a cervicalrib or dysfunction of the scalene may be irreversible but thestenosis due to abnormal breathing patterns and abnormalposture can be reversible (Edgelow 2004).

The third concept that Edgelow stresses is the conceptof fluid dynamics. As structural and fluid changes causerestriction in the size of the thoracic outlet they also causechanges in the pressure gradient, which also effects the

local neural circulation and the venous and lymphaticreturn to the whole upper extremity.

CONCLUSION

Communication between the referring physician andphysical therapist is a necessity to assure positive out-comes. Many authors combined treatment of soft tissuesand joints with neural tissue treatment (Edgelow 2004).This management includes posture correction, treatmentof affected structures including nerve excursions, muscu-lar, articular, as well as addressing the emotional compo-nent, which is necessary for successful outcomes.

The goal of treatment is to teach the patient to open upthe space between the clavicle and first rib by stretchingtight muscles, strengthening weak musculature, decreasenerve tension in the upper quadrant, improve tempera-ture differences in the hand, improve diaphragmaticbreathing and increase spinal mobility in the cervical-thoracic area. A clear understanding and interpretationof the provocative test are necessary for successful out-comes. The patient must realize that a period of 6 monthsor longer may be necessary to make a lasting effect ontheir symptoms.

As we manage patients, I have found that patients per-form stretching exercises without using proper techniques.Most patients do not understand that lateral flexion, with-out stabilizing the first rib, continues to add additionalcompression and tension in the scalene muscles. Patientsmust be instructed in lateral flexion with slight rotationalong with using a towel or a strap to hold the rib in acaudal position.

A total wellness concept of good eating habits and aero-bic conditioning should also be followed. Many TOSpatients are in poor aerobic condition causing decreasedrespiratory function and overuse of the scalene, trapeziusand sternocleidomastoid muscles. Postural correction,including spinal extension, will allow better chest expan-sion with inspiration resulting in diaphragmatic excursionand will decrease the use of the accessory respiratory mus-cles (Mackinnon & Novak 2002).

Clinical experience has shown that by identifying themechanical origin of symptoms, a successful treatmentprogramme consisting of symptom alleviation is mosthelpful along with empowering the patient to be in chargeof their own symptoms. Educating the patient in properposture and breathing patterns at both work and leisureis the cornerstone for designing a treatment programme.Physical therapy that addresses postural abnormalities,neural mobility, joint mobility, and muscle imbalancesis effective in relieving symptoms of TOS.

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