Thoracic Outlet Syndrome: A ComprehensiveReview of Pathophysiology, Diagnosis, andTreatment.Mark R. Jones, Harvard Medical SchoolAmit Prabhakar, Emory UniversityOmar Viswanath, Valley Anesthesiology and Pain ConsultantsIvan Urits, Harvard Medical SchoolJeremy B. Green, Louisiana State UniversityJulia B. Kendrick, Louisiana State UniversityAndrew J. Brunk, Louisiana State UniversityMatthew R. Eng, Louisiana State UniversityVwaire Orhurhu, Harvard Medical SchoolElyse M. Cornett, Louisiana State University

Only first 10 authors above; see publication for full author list.

Journal Title: Pain and TherapyVolume: Volume 8, Number 1Publisher: Springer (part of Springer Nature): Fully open access journals -CC BY-NC | 2019-04-29, Pages 5-18Type of Work: Article | Final Publisher PDFPublisher DOI: 10.1007/s40122-019-0124-2Permanent URL: https://pid.emory.edu/ark:/25593/tqt6k

Final published version: http://dx.doi.org/10.1007/s40122-019-0124-2

Copyright information:© The Author(s) 2019This is an Open Access work distributed under the terms of the CreativeCommons Attribution-NonCommercial 4.0 International License(http://creativecommons.org/licenses/by-nc/4.0/).

Accessed November 13, 2021 4:43 AM EST

REVIEW

Thoracic Outlet Syndrome: A Comprehensive Reviewof Pathophysiology, Diagnosis, and Treatment

Mark R. Jones . Amit Prabhakar . Omar Viswanath . Ivan Urits .

Jeremy B. Green . Julia B. Kendrick . Andrew J. Brunk .

Matthew R. Eng . Vwaire Orhurhu . Elyse M. Cornett .

Alan D. Kaye

Received: December 10, 2018 / Published online: April 29, 2019� The Author(s) 2019

ABSTRACT

Thoracic outlet syndrome, a group of diversedisorders, is a collection of symptoms in theshoulder and upper extremity area that resultsin pain, numbness, and tingling. Identificationof thoracic outlet syndrome is complex and athorough clinical examination in addition toappropriate clinical testing can aide in diagno-sis. Practitioners must consider the pathology ofthoracic outlet syndrome in their differentialdiagnosis for shoulder and upper extremity painsymptoms so that patients are directed

appropriately to timely therapeutic interven-tions. Patients with a definitive etiology whohave failed conservative management are idealcandidates for surgical correction. This manu-script will discuss thoracic outlet syndrome,occurrence, physical presentation, clinicalimplications, diagnosis, and management.

Keywords: Brachial plexus; Neurogenicthoracic outlet syndrome; Subclavian vein;Thoracic outlet syndrome

INTRODUCTION

Thoracic outlet syndrome (TOS) constitutes agroup of diverse disorders that result in

Enhanced Digital Features To view enhanced digitalfeatures for this article go to: https://doi.org/10.6084/m9.figshare.7951541.

M. R. Jones (&) � I. Urits � V. OrhurhuDepartment of Anesthesia, Critical Care and PainMedicine, Harvard Medical School, Beth IsraelDeaconess Medical Center, Boston, USAe-mail: mjones13@bidmc.harvard.edu

A. PrabhakarDivision of Critical Care, Department ofAnesthesiology, Emory University School ofMedicine, Atlanta, GA, USA

O. ViswanathValley Anesthesiology and Pain Consultants,Phoenix, AZ, USA

O. ViswanathDepartment of Anesthesiology, CreightonUniversity School of Medicine, Omaha, NE, USA

O. ViswanathDepartment of Anesthesiology, University ofArizona College of Medicine-Phoenix, Phoenix, AZ,USA

J. B. Green � J. B. Kendrick � A. J. Brunk �M. R. Eng � A. D. KayeDepartment of Anesthesiology, LSU Health SciencesCenter, New Orleans, LA, USA

E. M. CornettDepartment of Anesthesiology, LSU HealthShreveport, Shreveport, LA, USA

Pain Ther (2019) 8:5–18

https://doi.org/10.1007/s40122-019-0124-2

compression of the neurovascular bundle exit-ing the thoracic outlet. The thoracic outlet is ananatomical area in the lower neck defined as agroup of three spaces between the clavicle andthe first rib through which several importantneurovascular structures pass; more detailedanatomical descriptions will correspond withdiscussions of the relevant pathology [1]. Thesestructures include the brachial plexus, subcla-vian artery, and subclavian vein. Compressionof this area causes a constellation of distinctsymptoms, which can include upper extremitypallor, paresthesia, weakness, muscle atrophy,and pain [2].

TOS classifications are based on the patho-physiology of symptoms with subgroups con-sistingofneurogenic (nTOS), venous (vTOS), andarterial (aTOS) etiologies [3]. Furthermore, eachone of these subgroups can be related to eithercongenital, traumatic, or functionally acquiredcauses [4]. Examples of congenital etiologiesinclude the presence of a cervical rib or ananomalous first rib. Traumatic causes mostcommonly include whip-lash injuries and falls.Functional acquired causes can be related tovigorous, repetitive activity associated withsports or work. Diagnosis of TOS is generallydependent on clinician familiarity of TOS cou-pled with an evaluation of symptoms andpatient-specific risk factors. Clinical suspicioncan then be confirmedwith provocative physicalexam maneuvers, radiographic, and/or vascularstudies. Because of the wide range of etiologiesand lack of expert consensus for diagnostic test-ing, the true incidence of TOS is difficult to dis-cern. Several articles report an incidence of 3–80/1000 [4]. Neurogenic TOS accounts for over 90%of the cases, followed by venous and arterial eti-ologies [3]. Historically, TOS presents withsymptom onset between the ages of 20–50 yearsold and is more prevalent in women [5].

With the wide range of multifactorial eti-ologies, it also makes sense that best-practicetreatments for TOS involve a comprehensiveand multi-disciplinary approach. Managementoptions can include surgery, lifestyle modifica-tion, pain management, anticoagulation, phys-ical therapy, and rehabilitation [6]. This articletherefore intends to review the most relevant,noteworthy, and up-to-date literature, and to

provide clinicians with a concise summary ofboth diagnosis and management for TOS. Acomprehensive electronic literature search(1970–2018) process was conducted that inclu-ded PubMed, EMBASE, and MEDLINE databases,and Google Scholar. Previous materials pub-lished in peer-reviewed journals and grey liter-ature were reviewed in a systematic manner.References cited in relevant articles were alsoreviewed. Search terms used included ‘‘thoracicoutlet syndrome’’ AND ‘‘imaging’’ OR ‘‘angiog-raphy’’ OR ‘‘diagnosis’’ OR ‘‘neurogenic’’ OR‘‘venous’’ OR ‘‘arterial’’ OR ‘‘NSAIDs’’ OR ‘‘phys-ical therapy’’ OR ‘‘surgery’’ OR ‘‘antidepressants’’OR ‘‘Raynaud’s’’ OR ‘‘neuropathy.’’

This article is based on previously conductedstudies and does not contain any studies withhuman participants or animals performed byany of the authors.

OCCURRENCE, PHYSICALPRESENTATION

Epidemiology

As previously stated, TOS may be subcatego-rized into neurogenic, venous, or arterial,depending on the structure responsible forproducing symptoms. nTOS is by far the mostcommon, representing about 95% of cases [3].The brachial plexus trunks or cords, originatingfrom nerve roots C5 to T1, are responsible.nTOS can be further divided into true or dis-puted TOS, with disputed reportedly represent-ing 95–99% of all neurogenic cases [7]. Thesymptoms of true and disputed nTOS are largelythe same, though objective findings from motornerve conduction studies and needle elec-tromyography are notably absent in the dis-puted variety. Venous TOS accounts for 3–5% ofcases and arterial TOS the final 1–2% [3]. Thesubclavian and axillary vasculature is impli-cated in arterial and venous TOS.

Both true and disputed nTOS are morecommon in women [3]. Teenaged to 60-year-oldfemales are most frequently affected by truenTOS [3]. Whereas true nTOS is primarily uni-lateral, the disputed variety is often bilateral [7].The lower brachial plexus is affected in about

6 Pain Ther (2019) 8:5–18

80% of patients with the disputed subtype,while the upper brachial plexus is compromisedin the other 20% [7]. Arterial TOS, a predomi-nantly unilateral condition, affects both gen-ders equally and more often affects youngadults [8]. Venous TOS also tends to be unilat-eral and is more common in men than women.Due to its association with repetitive upperextremity activity, vTOS is more common inyounger, able-bodied individuals, and mostoften affects the dominant upper extremity [8].

Anatomy

Clinicians need to maintain familiarity with therelevant anatomy to fully conceptualize TOS.The thoracic outlet comprises the space fromthe supraclavicular fossa to the axilla. Thesymptoms of TOS arise from compression of thebrachial plexus nerves, subclavian artery andvein, and axillary artery and vein.

Described in Table 1 and diagrammaticallyrepresented in Fig. 1, the areas within the

thoracic outlet where compression of nerves orvasculature occurs include the interscalene tri-angle, costoclavicular space, and subcoracoidspace [7]. The interscalene triangle is the mostmedial compartment, and its borders are cre-ated by the anterior scalene muscle anteriorly,middle scalene muscle posteriorly, and first ribinferiorly. The brachial plexus and subclavianartery pass through the interscalene triangle,however the subclavian vein courses anterior tothe compartment [9]. The second compart-ment, the costoclavicular space, is bordered bythe subclavius muscle anteriorly and claviclesuperiorly. The first rib and anterior scalenemuscle form the inferior and posterior borders.The brachial plexus, subclavian artery, andsubclavian vein all pass through this compart-ment. The final and most lateral compartmentis the subcoracoid space. This space has alter-natively been labeled as the retropectoralisspace or the subcoracoid pectoralis minor space[9, 10]. The pectoralis minor muscle forms theanterior border of this space, and the ribs formthe posterior boundary. As its name wouldsuggest, the coracoid is located superior to thisspace. The brachial plexus passes through thesubcoracoid space, and the subclavian arteryand vein continue through it as the axillaryartery and vein.

Etiology

Numerous mechanisms elicit the characteristicpathology of TOS, including trauma, repetitivemotions, and anatomic variations. Traumaticevents are typically high velocity, most often inthe setting of a motor vehicle accident. Hem-orrhage, hematoma or displaced fracture candirectly compress the nerves or vasculature.Midshaft clavicular fracture in particular is arecognized cause [8]. Even after the initialinsult, fibrosis can develop and produce symp-toms [7]. Whiplash injuries exhibit a knownassociation with TOS, most often of the neuro-genic subtype; patients with a cervical rib arereportedly predisposed to this outcome [11].

Repetitive motions can lead to musclehypertrophy that contributes to compression.Additionally, overuse injury in the setting of

Table 1 Anatomic spaces of thoracic outlet syndrome

Compartment Borders Contents

Interscalene

triangle

Anterior: anterior scalene

muscle

Posterior: middle scalene

muscle

Inferior: first rib

Brachial

plexus

Subclavian

artery

Costoclavicular

space

Anterior: subclavius

muscle

Inferoposterior: first rib

and anterior scalene

muscle

Superior: clavicle

Brachial

plexus

Subclavian

artery

Subclavian

vein

Subcoracoid

space

Anterior: pectoralis minor

muscle

Posterior: ribs 2–4

Superior: coracoid

Brachial

plexus

Axillary

artery

Axillary

vein

Pain Ther (2019) 8:5–18 7

repetitive movements can cause swelling, smallhemorrhages, and subsequent fibrosis, whichcan also account for symptoms. Venous TOS isalso possible following repetitive motion.Paget–Schroetter disease, also called ‘‘effortthrombosis,’’ involves axillary or subclavianvenous thrombosis following strenuous repe-ated activity with the arms [12].

Myriad anatomic variations incite TOS. Onesuch variation, the presence of a cervical rib,bears an estimated prevalence of 1–2% of thegeneral population but remains asymptomaticfor most people. Patients with a cervical rib areat higher risk of nTOS, with up to 20% of nTOScases attributable solely to the presence of acervical rib [7]. Presence of a cervical rib is also apredisposing factor in the development of

arterial TOS, as it can compress the subclavianartery and cause stenosis or aneurysm [11].Congenital variations in musculature have alsobeen reported to cause TOS. For instance, asupernumerary scalene muscle may contributeto compression within the interscalene triangle[7].

Malignancy causing compression is anotherwell-documented etiology of TOS. Pancoasttumors, also known as superior pulmonary sul-cus tumors, can invade and compress the bra-chial plexus [13]. Benign tumors are alsocapable of producing the characteristic symp-toms, as illustrated by a rare case of multiplehereditary exostosis causing combined venous,arterial, and nTOS secondary to large osteo-chondromas [14].

Fig. 1 Thoracic outlet and relevant anatomy

8 Pain Ther (2019) 8:5–18

CLINICAL IMPLICATIONS

Prompt recognition of the presenting signs ofTOS is crucial to prevent long-term sequelae,specifically chronic upper extremity pain andsevere disability. In each subtype of TOS, anunderstanding of the causative anatomic aber-rancy can guide diagnosis.

Neurogenic TOS is caused by compression ofthe C5 through T1 brachial plexus nerve rootsand comprises up to 90% of total TOS cases [15].Compression of the nerve roots most oftenoccurs within the scalene triangle but can alsooccur in the subarachnoid space as the nerveroots traverse beneath the pectoralis minortendon. In this scenario, congenitally anoma-lous anatomy such as aberrant scalene muscu-lature, cervical ribs, and connective tissue maycompress and entrap nerve roots [16]. Addi-tionally, acquired anatomical variation, e.g.,scarring from injury, can affect these nerveroots. Accordingly, nTOS is often seen in young,active individuals who participate in athleticactivities that involve repetitive overhead upperextremity motion and heavy lifting [11]. Diag-nosis of nTOS is thereby based on the history ofsymptom presentation and clinical exam find-ings. Patients with nTOS often report consis-tently reproducible symptoms whenperforming the responsible activities anddemonstrate positional exacerbation whenmimicking these specific upper extremitymotions. Symptoms generally correspond sec-ondary to the level of nerve compression, withthe most common being upper extremityheaviness with above-the-shoulder activities. Asystematic review by Sanders et al. [11] descri-bed symptom distribution in neurogenic TOS toinclude upper extremity paresthesia (98%),neck pain (88%), trapezius pain (92%), shoulderand/or arm pain (88%), supraclavicular pain(76%), chest pain (72%), occipital headache(76%), and paresthesias in all five fingers (58%),the fourth and fifth fingers only (26%), or thefirst, second, and third fingers. In upper plexusTOS, involving compression of the C5, C6, andC7 nerves, pain is most often described in thelateral neck, with radiation superior to the earand occiput. Pain may also radiate posteriorly to

the rhomboid area, anteriorly across the clavicleinto the upper pectoral region, laterally throughthe deltoid and trapezius muscle areas, anddown the outer aspect of the arm [17]. In gen-eral, patients present with lower plexus TOSrather than upper, which corresponds to com-pression of the C8 and T1 nerves. Pain is typi-cally distributed along the posterior of anteriorshoulder with radiculopathy down the arm in amedio-brachial distribution along the inneraspect of the arm. Paresthesia tends to affect anulnar nerve distribution along the ring and littlefingers. Despite this etiological understandingof pathoanatomy, differentiation from othercervicobrachial symptoms may still prove chal-lenging difficult [18].

Venous TOS, also referred to as Paget–vonSchroetter syndrome, comprises 10–15% ofcases, and is caused by subclavian compressionwithin the costoclavicular space [19]. Mechani-cal compression and repetitive injury of thesubclavian vein between the clavicle and firstrib can lead to abrupt blood flow stagnation andsubsequent effort thrombosis. This causes thepathognomonic presentation of acute upperextremity swelling, cyanosis, heaviness, andultimately pain. Raynaud’s-like symptoms maybe appreciated with vTOS but are typicallyunilateral, unlike the former disease [20]. It isimportant to remember, however, that Ray-naud’s itself may present as unilateral in * 7%of cases, thus the clinician need maintainawareness of other causes of vascular compro-mise in their approach [21]. Like nTOS, venousTOS occurs frequently in physically activeindividuals, aged 15–45, many of whom par-ticipate in work or recreational activities thatinvolve heavy lifting and repetitive upperextremity overhead motion. Pulmonary embo-lism is an important complication of venousand occurs in 10–20% of patients. In compar-ison to lower extremity DVT, however, clotburden is typically minimal and infrequentlylife-threatening, as extrinsic mechanicalobstruction of blood flow theoretically preventsproximal embolization of venous blood clot.Though patients with effort thrombosis mayinitially present with an abnormal coagulationprofile, genetic hypercoagulable parameters aretypically negative, thusly distinguishing vTOS

Pain Ther (2019) 8:5–18 9

as a mechanical problem rather than a pro-co-agulative hematologic disorder [22, 23]. Assubclavian vein thrombosis may arise fromalternative etiologies, imaging such as venousduplex, MRI, and CT can assess the proximalsubclavian vein status to confirm the mechani-cal diagnosis [19]. Differentiation from nTOS isclinical; in contrast to pain exacerbated byoverhead upper arm positioning, the symp-tomatology of venous thrombosis is stable.

Arterial TOS is by far the most rarelyobserved, occurring in 2–5% of TOS cases. Sub-clavian artery compression within the scalenetriangle may be caused by an anomalous firstrib, which ultimately developing an aneurysmdistally. Acquired types may also be seen inphysically active patients and athletes in whomarterial entrapment may occur at the level ofthe pectoralis minor tendon and the humeralhead [24]. Arterial compression incites intimaldamage, turbulent blood flow, and vessel dila-tion. Eventual arterial thrombosis and distalembolization may result in acute distal upperextremity ischemia. Clinical features are pri-marily vascular, as discussed, with secondaryneurologic abnormalities as sequelae.

Clinicians should recall TOS on their differ-ential diagnosis when confronted with a patientsuffering from upper extremity pain and sup-porting physical exam findings. Adult patientswho present with features of TOS necessitate alow threshold for imaging, as delay in treatmentcan lead to irreversible changes and chronicpain. While nTOS is the most frequent subtype,its diagnosis may be the most challenging bythe lack of readily apparent clinical findings,such as vascular abnormalities on radiography[18].

Diagnosis of TOS is further complicated byalternative disorders with similar presentation.Nerve compression at the cervical spine orelbow and wrist, involving the median andulnar nerve, may occur in conjunction withTOS. A presentation as such is referred to asdouble crush syndrome and may mask the pre-sentation of TOS [25]. In these patients, carefulconsideration of multiple imaging modalities,electromyographic studies, and detailed physi-cal examination are crucial to discern the foci ofneurovascular compromise. Despite this, in as

many as 29% of patients who present withsymptoms consistent with distal peripheralnerve entrapment syndromes (e.g., carpal tun-nel syndrome), there is no evidence of clinicalor physical exam findings supporting a distalnerve lesion [26]. Furthermore, in patients withelectrophysiologically proven distal entrapmentsyndrome, proximal neurological lesions at thelevel of the cervical spine may contribute tosymptoms; in a review of 1000 cases of carpaltunnel syndrome, 89% of patients exhibitedconcomitant cervical arthritis, which is capableof eliciting similar symptoms [27]. Likewise, in astudy of cyclists with ulnar nerve neuropathy,proximal neural lesions contributing to a dou-ble crush syndrome were symptomaticallycontributory [28]. The prevalence and diagnosisof nTOS is controversial, and much debate sur-rounds the role of nTOS to upper limb entrap-ment neuropathies. Careful considerationshould, therefore, be given to compressiveneuropathies at distinct, alternative sites whichcan lead to similarly disabling upper extremitypain and weakness.

Owing to the high prevalence of carpal tun-nel syndrome (CTS), the concurrence of TOSwith CTS has been extensively examined.However, controversy remains in terms of dou-ble crush phenomenon pathology, diagnosis,and treatment of these two syndromes. TOS israre, and diagnosis often lacks specificity.Moreover, carpal tunnel syndrome is ofteninaccurately diagnosed. Compounded, theoccurrence of simultaneous TOS and CTSbecomes exceedingly rare. As such, it is unlikelythat the combination would precipitate doublecrush syndrome [29]. In patients with persistentsymptoms following decompression of distalnerve entrapment, though TOS may not beentirely excluded, proximal nerve compressionstemming from cervical radiculopathy may bethe more likely etiology. While reports havedemonstrated TOS as a contributing factor todouble crush phenomena with distal entrap-ment neuropathies, the prevalence of TOS inCTS is around 1% [30–33]. Furthermore,although the presence of double crush syn-drome is difficult to confidently diagnose, thefact that CTS is a highly accepted diagnosis mayexplain the elevated incidence of reported

10 Pain Ther (2019) 8:5–18

coincident CTS with TOS. The association ofTOS with CTS is both plausible and previouslydocumented, but the unpredictability of bothsyndromes warrants surgical treatment of thedistal compressive neuropathy first [32]. Persis-tent entrapment neuropathy following surgicaltreatment for TOS should raise suspicion fordistal nerve entrapment syndrome [34]. Com-plete resolution of symptoms is achievable onlyby addressing all points of suspected neuralcompression [35, 36].

Though inherently distinct etiologically, thethree forms of TOS share a fundamental mech-anism of extrinsic neurovascular compressionthat ultimately produces severe pain and dis-ability. In all cases, early recognition and diag-nosis is crucial to initiation of the propertreatment. TOS remains a challenging andhighly controversial diagnosis, and alternative,and possibly coincidental, proximal or distalcompressive neuropathies must be excluded.

DIAGNOSIS AND MANAGEMENT

Relevant Physical Examination

When suspecting TOS, a general physical examshould focus on a thorough examination of notonly the shoulder and upper extremity but thecervical spine as well, with particular attentionto head and neck posture. A careful comparisonbetween the affected and contralateral extrem-ity can reveal obvious signs of wasting andweakness, while more subtle differences in skincolor, temperature, and hair distribution mayalso be evident. Depending on the underlyingetiology, patients may present with varied yetcharacteristic physical exam findings of theunderlying cause of obstruction. Vascular TOScan cause large differences in blood pressurereadings between arms ([ 20 mmHg); theshoulder and chest may appear edematous invTOS, while the upper extremity may appearpale or cyanotic with aTOS [37]. Not surpris-ingly, nTOS yields more obvious signs of mus-cular atrophy such as the Gilliatt–Sumner hand,which is a constellation of atrophic abductorpollicis brevis, hypothenar, and interosseimuscles [38]. Other notable physical exam

findings may include supraclavicular fullness oraneurismal pulsations [39].

While the use of individual provocativemaneuvers for the diagnosis of TOS has led to ahigh number of false positives, studies indicatethat reliance on multiple tests in conjunctionmay increase the specificity of TOS identifica-tion. Table 2 below describes commonly usedmaneuvers in the physical exam [39, 40]. Astudy by Gillard et al. demonstrated that com-bining the Adson and Roos test increased thespecificity from 76 to 30% when used alone to82% when both are positive [41].

Diagnostic Modalities

Further diagnostic testing is directed predomi-nantly by clinical symptoms and the type ofsuspected TOS. While testing is often equivocalor negative in nTOS, making it a diagnosis ofexclusion, testing for vTOS focuses on thedemonstration of stenosis or occlusion of sub-clavian vessels. Below are tests commonly usedin diagnosis and surgical planning for appro-priate candidates.

Electrodiagnostic Testing

Although a majority of patients will have nor-mal or negative results, electrophysiologicalevaluation via nerve conduction and EMG isindicated for those suspected of nTOS. How-ever, when positive nTOS presents with a char-acteristic pattern of nerve conductionabnormalities. Sensory response may be normalin the median distribution but diminished orabsent in medial antebrachial cutaneous andulnar sensory responses. Additionally, dimin-ished or absent median and ulnar motorresponse may be seen, typically with a moreprofound decrease in the median response.These findings are highly suggestive of nerveconduction abnormalities involving the C8 andT1 fibers (T1 usually more affected than C8) andserve to rule out cervical radiculopathy andmyelopathy [10, 42, 43].

Injection of local anesthetic into the anteriorscalene muscle has been used to successfullydiagnose nTOS. Temporary relief of symptoms

Pain Ther (2019) 8:5–18 11

following medication injection decreases mus-cular tension on the neural bundle and maypredict response to surgical decompression. Inthose with a positive response to the block, 94%were shown to have a positive outcome fol-lowing surgical correction as compared to only50% of patients who underwent decompressionfollowing a failed block [39].

Imaging

Imaging can also be helpful in confirming sus-pected cases of TOS. Anatomical abnormalitiesor defects, such as prominent cervical ribs,fracture calluses, or compressive tumors arecommonly demonstrated on chest, shoulder, orspine radiographs. Conventional arteriographyand venography, while they may demonstrateextrinsic compression, do not permit a cleardepiction of the impinging anatomic structure,and they tend to be replaced by less invasiveprocedures (CT, MR imaging, sonography) asdescribed below [17]. In addition to electrodi-agnostic testing, MR neurogram can providefurther detail to identify anatomical relation-ships or particular sites of compression.

For suspected vascular TOS, ultrasoundmaintains high sensitivity and specificity, isnoninvasive and inexpensive, and should be

the initial imaging test of choice. CT or MRangiography can differentiate equivocal cases orprovide additional anatomic detail required forsurgical planning [37].

Conservative Management Strategies

Management strategies depend on the under-lying etiology of TOS. Initial treatment of nTOSconsists of conservative measures, whereasvTOS or nTOS with refractory symptoms mayundergo surgical management. Treatment isreserved only for symptomatic patients, as thepresence of a cervical rib exists in 0.5% of thepopulation but only a small fraction developsymptoms [38].

A consensus on the appropriate conservativeregimen for nTOS remains controversial. How-ever, a multimodal treatment approach includ-ing patient education, TOS-specificrehabilitation, and pharmacologic therapieshave shown positive results. Rehab is recom-mended as the initial nonsurgical managementfor nTOS and should include patient education(postural mechanics, weight control, relaxationtechniques), activity modification, and TOS-fo-cused physical therapy (active stretching, tar-geted muscle strengthening, etc.) [38]. Onestudy demonstrated symptomatic relief in 25 of

Table 2 Common provocative diagnostic tests for thoracic outlet syndrome

Test Maneuver Result

ADSON TEST Affected arm is abducted 30� at the shoulderwhile maximally extended. While extending the

neck and turning head towards ipsilateral

shoulder, patient inhales deeply

Decrease or absence of ipsilateral radial pulse

Elevated Arm

Stress Test

(EAST) or

ROOS

Arms are placed in the surrender position with

shoulders abducted to 90� and in external

rotation, with elbows flexed to 90�. Patientslowly opens and closes hand for 3 min

Precipitates pain, paresthesias, heaviness or

weakness

Upper Limb

Tension Test

(ULTT) or

ELVEY

Position 1: arms abducted to 90� with elbows

flexed

Position 2: active dorsiflexion of both wrists

Position 3: head is tilted ear to shoulder, in both

directions

Positions 1 and 2 elicit symptoms on the

ipsilateral side, while position 3 years elicits

symptoms on the contralateral side

12 Pain Ther (2019) 8:5–18

42 patients with nTOS following 6 months ofphysical therapy [37].

Pharmacologic interventions often providesymptomatic relief, and primarily includeanalgesics (NSAIDs and/or opioids) for neuro-pathic pain, as well as muscle relaxants, anti-convulsants, and/or antidepressants asadjuvants [6]. Additionally, injection of localanesthetic, steroids, or botulinum toxin type Ainto the anterior scalene and/or pectoralismuscle have demonstrated varying levels ofsuccess in observational studies [44], althoughthe use of BTX-A failed to demonstrate signifi-cant benefit in a randomized trial [45].

SURGICAL MANAGEMENTSTRATEGY IN FAILEDCONSERVATIVE MANAGEMENTAND TREATMENT OUTCOMES

Surgery for TOS is reserved for patients whohave failed conservative management. Thethreshold for decompression varies widely formild to moderate symptoms, but certainsymptoms require surgery.

As previously discussed, physical therapyand conservative management of nTOS shouldpersist for at least 4–6 months prior to consid-eration of surgical intervention [46]. However,for patients with arterial or venous TOS, theinitial intervention is most often surgical. A trialof anticoagulation via catheter-directed throm-bolysis and systemic heparin therapy may befirst attempted for patients with arterial or vas-cular TOS [47]. In cases of mild upper extremityischemia, catheter-directed thrombolysis mayrestore perfusion. Symptoms refractory to thesemeasures require surgery.

Surgical candidates should have failed con-servative management [40]. Most surgical can-didates exhibit nTOS with uncontrolled pain orprogressively worsening upper extremity weak-ness. The surgery of choice is a first rib resectionaimed at brachial plexus decompression, typi-cally performed by vascular surgeons. Theoperation can also be performed by thoracicsurgeons, neurosurgeons, orthopedic surgeons,and plastic surgeons [46]. In nTOS, the first rib

is removed in addition to a scalenectomy orscalenotomy.

The three approaches to brachial plexusdecompression by first rib removal includetransaxillary, supraclavicular, and infraclavicu-lar techniques. Each approach has achievedgood outcomes, with no definitively superiortechnique [48]. While the transaxillary andsupraclavicular approaches are utilized morefrequently, technique is often chosen based onthe individual patient and unique anatomicalconsiderations. The supraclavicular approachrequires a scalenectomy of the middle andanterior scalene muscles to expose a small por-tion of the first rib. The compression is therebyeasily exposed, allowing for access to the bra-chial plexus if neurolysis is indicated. Thetransaxillary approach is performed by access-ing the first rib between the pectoralis majorand latissimus dorsi in the axilla. With thepatient in the lateral position, careful dissectionof the axillary vasculature and nerves mayexpose the first rib. In this approach, exposure islimited and potential brachial plexopathy mayoccur through over-manipulation and retrac-tion. Less common, the infraclavicularapproach allows for vascular reconstruction inpatients with venous or arterial TOS and shouldbe pursued if central venous exposure isrequired.

Brachial plexus injury after first rib resectiondoes occur, but reporting varies widely [49]. In amulti-institution database study, brachialplexus injuries were reported in 0.6% patientswith nTOS following transaxillary first ribresection [50]. However, another study oftransaxillary first rib resections in patients withnTOS reported a brachial plexus injury inci-dence of 9%, with an incidence of 4% aftersupraclavicular first rib resection [51].

More recently, the introduction of mini-mally invasive techniques has achieved superioroutcomes in first rib removal, as both roboticand thoracoscopically assisted approachesminimize brachial plexus manipulation [46].Additional training, equipment, and expertise isrequired but may limit the overall surgical risk.

Overall outcomes from surgical decompres-sion are very positive. Following surgical inter-vention, 95% of patients with nTOS reported

Pain Ther (2019) 8:5–18 13

‘‘excellent’’ results [52]. In a 5-year follow-upstudy of patients with vTOS, patency rates werebetter than 95% [53]. Impediments to successfuloutcomes include major depression or comor-bid conditions that skew the initial diagnosis[53].

RECENT DEVELOPMENTS

Asmore patients receive diagnosis and treatmentfor TOS, the referral pattern has changed. Insteadof evaluation and treatment by multiple disci-plines before consideration of TOS, patients arenow referred sooner despite a shorter duration ofsymptoms, which improves the predictedresponse to surgical treatment [3]. Additionally,a rise in the number of adolescent cases has beendescribed, owing to repetitive or vigorous activ-ity such as musical instrument or athleticendeavors. More common in adolescents thanadults, first rib resection has been successfullyand safely performed for vTOS and aTOS withgood outcomes and fast recovery [54].

Since TOS is a rare and complex group ofdisorders with potentially severe and disablingsymptoms, care can be challenging for healthcare providers. Therefore, a systematic, orga-nized approach to the diagnosis and treatmentof TOS provides an opportunity for specialists todeliver patient-centered care and achieve opti-mal results. This specialized type of care is bestdelivered through the efforts of a multi-disci-plinary team that consists of various specialists,including vascular surgery, thoracic surgery,neurology/neurosurgery, orthopedics, radiol-ogy, anesthesiology, pain management, physi-cal therapy, and occupational therapy [55]. Forthis reason, centers of excellence for TOS havebeen established around the country withdemonstrable improvements in outcomes [3].

Venous and arterial TOS are diagnosed by acombination of clinical presentation andimaging. Ongoing developments in the diag-nosis of TOS include dynamic CT angiography,MR neurography, and Diffusion Tensor Imaging(DTI). These imaging modalities can be used toidentify brachial plexus branching variants inwhich susceptibility to compression by thescalene muscle is increased. Neurogenic TOS is

generally more difficult to diagnose as nerveand tissue inflammation lack consistent radio-graphic evidence. However, as imaging studiesevolve, newer modalities with higher qualityallow for improved diagnostic objectivity [56].MRI can evaluate the anatomy of the thoracicoutlet, the soft tissue structures causing com-pression, and allow direct visualization of bra-chial plexus compression [40]. Magneticresonance neurography (MRN) is an imagingmodality that allows non-invasive visualizationof nerve morphology and signal. In this tech-nique, signals from surrounding soft tissue suchas adipose are suppressed, and pulsation artifactfrom pulsating blood is removed. Continuedimprovements in high-resolution MRN may,therefore, augment current diagnostic modali-ties by facilitating prompt identification ofbrachial plexus compression across the thoracicoutlet in patients with nTOS [57].

While MRN denotes a class of techniquesintended for assessment of peripheral nerves,diffusion tension imaging (DTI) or tractographyis reserved for the CNS [58]. Short tau inversionrecovery (STIR) sequences and the spectral adi-abatic inversion recovery (SPAIR) preparatorymodule are variations of MRN and deliver amore complete anatomical description of thenerves comprising the brachial plexus. DTIsequences to visualize nerve fascicles areemployed in the modeling technique of trac-tography, allowing for a more comprehensiveassessment of peripheral nerve injury [57]. Onestudy regarding MRN demonstrated a 100%positive predictive value in all 30 patientsinvolved; however, ultrasound also identifiedcompression all patients with nerve lesionsvisualized on MRN [59].

Current mainstays of diagnosis includeduplex ultrasound, arteriography, hemody-namic testing (finger plethysmography) at restand with symptom-producing maneuvers, aswell as CT and MR angiography [60]. Invasivearteriography and angiography are useful in thedetection of complications from aTOS such asthrombosis, embolization, and aneurysm. Theinvasive nature of these techniques limits theiruse to surgical planning rather than pure diag-nostics. Other non-invasive tests such as MRand CT angiography are more readily employed

14 Pain Ther (2019) 8:5–18

for their diagnostic utility outside of surgicalplanning. Dynamic testing allows the clinicianto evaluate arterial compression with provoca-tive maneuvers, while imaging helps to definethe anatomic source of compression and con-firm the diagnosis of arterial, venous, or nTOS[40].

Surgical Advancements

As noted above, first rib resection with scalenec-tomy remains the operation of choice fordecompression, but as surgical advancementscontinue to emphasize minimally invasiveapproaches, some institutionsnowemployVATSin order to achieve a clearer visualization of theoperative field and potentially minimize injuryto the neurovascular bundle [61]. Two additionalstrategies, the robotic-assisted and endoscopic-assisted trans-axillary approaches, are noveltechniques with potential benefit, the latteraiming to decrease risk of pneumothorax [56].

FUTURE DIRECTIONS

The past 50 years have welcomed substantialprogress in terms of our understanding andtreatment of TOS, but several knowledge gapsremain elusive. Diagnosis, for instance, presentsa considerable challenge to this day. A reliableand objective diagnostic tool, such as imaging,would herald a new era for patients with TOS[3]. Preoperative MRI or CTA comparison ofpatients with TOS to control patients has beensuggested as a promising avenue of research.Similarly, timing of post-operative imaging is asubject of debate, with various schedulesemployed across institutions. For example,venograms at 2 weeks after first rib resectionand scalenectomy may encounter residual post-surgical inflammation; the precise timing post-surgical venography requires further investiga-tion [3].

Lastly, the impact of prosthetic versusautologous tissue for aTOS reconstruction hasyet to be elucidated. Comparative patency ratesand need for reoperation have not been firmlydelineated, are further research in this areawould provide significant benefit, although the

inherent rarity of aTOS renders large, multi-center investigations complex [3].

CONCLUSIONS

Since the first use of the term TOS by Peet et al.,there have been significant advancements in theunderstanding and treatment of the syndrome.The upper extremity pain and numbness typicalof the condition have been subcategorized intodistinct disorders based on the structuresinvolved. A history of trauma or repetitivemotions combined with supportive physicalexam findings suggests the correct diagnosis.Other diagnostic modalities such as MRI, ultra-sound, and nerve conduction studies can furthersupport the diagnosis, and ongoing develop-ments in this sphere are currently underway.

Despite advances, substantial controversyregarding the diagnosis remains. This is evi-denced by the lack of objective findings sur-rounding nTOS, the most common and widelydisputed form of TOS. The challenges associatedwith diagnosis complicate the selection of theappropriate treatment option. In some cases,e.g., acute vascular insufficiency or progressiveneurologic dysfunction, surgical decompressionis clearly indicated. Prompt recognition andtreatment of TOS provide the greatest opportu-nity for optimal recovery. Unfortunately, themultitude of nonspecific symptoms and chal-lenges in diagnosis can delay treatment andincrease the risk of complications.

Surgical intervention for TOS syndrome isreserved for patients who have failed conserva-tive management. Conservative treatmentincluding physical therapy need be trialed for atleast 4–6 months prior to consideration of sur-gical intervention [46]. Definitive therapy forpatients with refractory aTOS or vTOS, however,remains surgical intervention.

ACKNOWLEDGEMENTS

Funding. No funding or sponsorship wasreceived for this study or publication of thisarticle.

Pain Ther (2019) 8:5–18 15

Authorship. All named authors meet theInternational Committee of Medical JournalEditors (ICMJE) criteria for authorship for thisarticle, take responsibility for the integrity ofthe work as a whole, and have given theirapproval for this version to be published.

Disclosures. Alan D. Kaye is a speaker forDepomed, Inc. and Merck, Inc. Mark R. Jones,Amit Prabhakar, Omar Viswanath, Ivan Urits,Jeremy B. Green, Julia B. Kendrick, Andrew J.Brunk, Matthew R. Eng, Vwaire Orhurhu andElyse M. Cornett have nothing to disclose.

Compliance with Ethics Guidelines. Thisarticle is based on previously conducted studiesand does not contain any studies with humanparticipants or animals performed by any of theauthors.

Open Access. This article is distributedunder the terms of the Creative CommonsAttribution-NonCommercial 4.0 InternationalLicense (http://creativecommons.org/licenses/by-nc/4.0/), which permits any noncommer-cial use, distribution, and reproduction in anymedium, provided you give appropriate creditto the original author(s) and the source, providea link to the Creative Commons license, andindicate if changes were made.

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