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Neurologic Thoracic Outlet Syndrome: Summarizing a Complex History and Evolution

Stewman, Chaney MD1; Vitanzo, Peter C. Jr MD2; Harwood, Marc I. MD3

doi: 10.1249/JSR.0000000000000038
Chest and Abdominal Conditions

Thoracic outlet syndrome (TOS) is a blanket term encapsulating many different clinical entities. Neurologic or neurogenic TOS (NTOS) is its main contributor, but it remains a complicated and sometimes controversial entity. NTOS incorporates numerous types, etiologies, clinical presentations, diagnostic findings, and therapeutic modalities. This article reviews the spectrum of disease within the thoracic outlet that affects the brachial plexus, with a special emphasis on the commonly afflicted sports medicine patient.

1Department of Family and Community Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA; 2Department of Family and Community Medicine, Jefferson Medical College, Thomas Jefferson University and Rothman Orthopaedic Institute, Jefferson Medical College, Philadelphia, PA; and 3Department of Family and Community Medicine, Jefferson Medical College, Thomas Jefferson University and Rothman Orthopaedic Institute, Jefferson Medical College, Philadelphia, PA.

Address for correspondence: Marc I. Harwood, MD, Family and Community Medicine, Thomas Jefferson University—Jefferson Medical College, 925 Chestnut St, 5th Floor, Philadelphia, PA 19107; E-mail:

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Historical Perspective and Evolution of Terminology

Five shoulder girdle syndromes related to neurovascular compression were described in the early 1900s based on the presumed mechanism of injury: cervical rib, first thoracic rib, scalenus anticus, costoclavicular, and subcoracoid-pectoralis minor (16,21,43). In 1945, Wright et al. termed neurovascular compromise at either the retroclavicular space or subcoracoid space a “hyperabduction syndrome,” which today is referred to as the entity pectoralis minor syndrome (PMS) (4,20,21,24,37,38).

In 1956, attempting to unify these terms, Peet et al. used the term thoracic outlet syndrome (TOS) (16,39,41,43). Classification by area of anatomical compromise was proposed in 1984 by Wilbourn, yielding the following major categories and subcategories that exist in the present day: vascular TOS (arterial and venous), neurologic TOS (true/classic and disputed, also referred to in literature as nonspecific, postural, assumed, or symptomatic), and neurovascular/combined (traumatic and disputed) (16,35,40,44). This classification system primarily excludes the previous recognition of PMS or any neurovascular compromise within the subcoracoid space of the thoracic outlet.

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True neurologic, arterial, venous, and traumatic TOS are extremely rare conditions, accounting for less than 5% of TOS cases (16,34,35). Disputed TOS seems to be the prevailing form of TOS, accounting for 95% to 99% of neurogenic TOS (NTOS) (11,26,35) and affecting up to 8% of the population (16). Prevalence data for PMS do not exist despite its recent reemergence within TOS literature.

True NTOS refers to a rare primarily unilateral disorder that afflicts predominantly females from late teens to 60 years of age (43,44). Its diagnostic criteria include the presence of a cervical rib from which fibrous bands extend to the first thoracic rib and cause stretching and compression of the proximal lower trunk of the brachial plexus (43). Consequently it produces a constellation of symptoms and signs found both on physical examination and by electrodiagnostic studies (EDX).

Disputed TOS most commonly affects the brachial plexus through either direct trauma or repetitive stress injury (RSI). There is a female predominance and it is frequently bilateral. Two subtypes exist based on whether the upper (20% of patients) or lower (80% of patients) brachial plexus is affected (14,16,44). Some clinicians and surgeons argue that this entity is not truly a TOS because it results in primarily subjective symptoms and instead believe that it falls better under a pain syndrome category or a musculoskeletal or peripheral nerve disorder (35,44). Others argue it being an underdiagnosed form of NTOS due to its subjective diagnostic criteria (35,44). This category of NTOS most commonly is termed “disputed TOS” in light of these arguments, although as described previously, it also has been referred to in literature by other descriptors: nonspecific, postural, assumed, or symptomatic.

Traumatic TOS is a rare primarily unilateral neurovascular injury within the thoracic outlet caused most commonly by a traumatic midshaft, displaced clavicle fracture (16,43,44). Most reported cases have occurred within the context of high-velocity motor vehicle accidents (7,15). High-level contact and speed sports involving falls have been implicated also, including rugby, skiing, and sky diving (7).

Although initially described long ago as within the spectrum of shoulder girdle syndromes, many practitioners to date have regarded PMS as separate from NTOS. PMS patients present similarly to those with disputed TOS as a result of a hyperextension injury or RSI, often due to overhead sports. Sanders et al. (32,33,37) argue that many patients who are being evaluated initially for NTOS have PMS either in isolation or concurrently, referred to as a “double crush syndrome.”

Neurologic TOS (NTOS) broadly refers to conditions of brachial plexus injury and compression. Classically NTOS referred to brachial plexus injury within the scalene triangle (33), but it now encompasses three anatomical areas of the thoracic outlet. Some believe that only true NTOS falls within its breadth, while others conclude that disputed TOS is its main contributor (26,30,35,44). Complicating matters, traumatic TOS also can cause rarely thoracic outlet neurovascular compromise, and PMS is an entity arguably within the TOS spectrum that appears to overlap with many patients initially diagnosed with NTOS (32,33,37,42,44).

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Anatomy of the Thoracic Outlet

Thoracic outlet anatomy (Figure) spans from the supraclavicular fossa to the axilla. Coursing through the thoracic outlet is the brachial plexus (C5 to T1 nerve fibers) and subclavian and axillary arteries and veins. The three subdivisions of the brachial plexus are determined by its anatomical relationship to the clavicle: supraclavicular, retroclavicular, and infraclavicular (16).



Three anatomical areas within the thoracic outlet can impart neurovascular compromise: interscalene triangle (demarcated by the borders of the anterior and middle scalene muscles and first rib), costoclavicular space (space between the clavicle and first thoracic rib), and subcoracoid space (also called the retropectoralis minor space or coracopectoral tunnel and defined as the space beneath the pectoralis minor tendon where it inserts on the coracoid process) (2,12–14,26,44).

The brachial plexus by convention is affected in the interscalene triangle in true NTOS, whereas it can be affected at all three of these anatomical locations in disputed TOS (14,44). The brachial plexus and subclavian vein and artery are all potentially compromised within the costoclavicular space in traumatic TOS, as is the the brachial plexus and axillary vein and artery within the subcoracoid space in PMS.

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The principal causes of NTOS are vast. Understanding thoracic outlet anatomy can facilitate a mastery of both etiologies and differential diagnosis of brachial plexus compression.

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Interscalene triangle narrowing

The presence of cervical ribs cause problems either through interscalene triangle narrowing or through a concurrent fibrous band causing direct compression, elongation, or angulation of the brachial plexus (14,16,18,44). It is surmised that only up to 20% of NTOS cases are solely due to the presence of a cervical rib. This is supported by the fact that cervical ribs (up to 1% to 2% of the general population (8,10,14,16,34)) are far more common than true NTOS (one person per million (3,16)).

Some individuals are born with a supernumerary scalene muscle within the interscalene triangle, referred to as the scalenus minimus muscle, scalenus pleuralis, scalenus accessories, scalenus anticus minor, or petit scalene (14,16,25). Its size is variable and its incidence remains a debate, with literature quoting vast ranges (7.8% to 71.7% of the general population by cadaver analysis) (25). Brachial plexus compression is postulated to occur when the scalenus minimus is well defined to overdeveloped (25).

Hyperextension injuries of the neck have been implicated, as in cases of falls or whiplash from motor vehicle accidents (15–17,26,34,35,44). RSI is a well-established contributor, specifically among factory workers or cases of prolonged sitting at a keyboard (16,26,34,35,42,44). Hyperextension of the scalene muscles acutely cause hemorrhage and swelling (15,17,26,35). Later, fibrosis and tightness can result, which is thought to create brachial plexus compression in NTOS (14,17,26,35).

Abnormal posture and repetitive overhead sports activities like swimming and tennis also have been proposed as a predisposing factor in NTOS, resulting in relative hypertrophy and atrophy of muscles within the neck (14,16,26,41,44). The hypothesis made by Ochsner et al. in 1935 regarding increased tone of the anterior scalene muscle (ASM) leading to TOS has been supported by a histologic study showing ASM type 1 (slow twitch) fiber predominance and hypertrophy, which reduces after tenotomy (22).

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Costoclavicular space narrowing

Abnormalities within the clavicle (e.g., callus formation from previous fracture) or inherent positions and mechanics that narrow the costoclavicular distance (e.g., shoulder abduction, shoulder extension or poor posture) can result in costoclavicular space narrowing (12–15,26,28). Sporting activities like archery that require repetitive and prolonged maintenance of the shoulder girdle in a fixed position with shoulder abduction and extension (the draw position) have been implicated as well, theorizing that this positioning results in brachial plexus impingement from costoclavicular space narrowing (28).

Cho et al. (11) supported the hypothesis that lower shoulder girdle positioning as determined by the radiographic position of the clavicle may be a risk factor in NTOS. Increased vertebrae visualization above the clavicle on lateral and frontal radiographs corresponded to a lower positioned shoulder girdle and was found to be more prevalent in patients with NTOS than their control group of carpel tunnel syndrome patients. Interestingly this may correspond to the long-standing observation that individuals with “long necks and droopy shoulders” are predisposed to NTOS (16,44).

Direct compression or injury of the brachial plexus by a fracture fragment in traumatic TOS can occur, as well as indirect injury through the presence of pseudoaneurysm or hematoma (16,43,44). Most cases have an acute presentation associated with high-velocity trauma. If clinical presentation is not immediate, it may be secondary to clavicle malunion or hypertrophic callus formation (16,43,44). Similar to NTOS, a histologic study showed that fibrosis within the scalene muscles is also an important part of traumatic TOS pathology (36).

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Subcoracoid space narrowing

A contracted, shortened pectoralis minor muscle (PMM) resulting in scapula abduction and shoulder girdle protraction creates subcoracoid space narrowing in PMS (40). Similar to disputed TOS, PMS cases have been described most commonly in motor vehicle accidents, falls, and RSI (37). Sports-related PMS also has been well described in overhead sport participants (33,37,38). Similar to data collected regarding scalene muscles, these events/injuries likely also create relative PMM hypertrophy, hemorrhage, swelling, and fibrosis.

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A thorough history and physical examination complemented by appropriate EDX and radiographic studies are paramount for diagnosis. Unfortunately no gold standard diagnostic testing exists for NTOS.

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The lower brachial plexus (C8–T1) is affected in true NTOS, compromising its innervated muscles and dermatomes. Complaints of hand weakness, atrophy, and loss of dexterity initially will bring most patients with this entity to seek medical attention (44). Patients often describe a preceding long history of intermittent medial upper extremity and forearm myalgias and paresthesias.

Clinicians and surgeons must rely on patient history and be comfortable with subjective reporting in order to diagnose disputed TOS and PMS. Sanders et al. (35) propose that NTOS be approached and managed similar to how clinicians approach migraine headaches that produce a constellation of symptoms frequently without objective findings.

Depending upon which rami are affected in disputed TOS, patients will report pain and paresthesias either in their head, neck, thorax, and shoulder (upper plexus; C5–C6) or neck, medial arm, forearm, and fourth and fifth digits of the hand (lower plexus; C8–T1) (14,16,26,44). Fatigue and weakness affecting muscles of the shoulder girdle or intrinsice muscles of the hand may also be present (44).

Patients report pain and paresthesias in similar distributions in PMS, localizing mostly to the anterior chest wall, trapezius muscle and hands, but can also extend to involve the neck, shoulder, axilla and arms (32,37). They often report that their upper extremity weakness and paresthesias are worsened by overhead activities (32,37,38,42). In the rare cases of traumatic TOS, upper extremity pain is nearly uniformly present with a known history of significant trauma (16,43,44).

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Physical examination

Motor function appears to be affected preferentially compared with sensory function in true NTOS, and thenar eminence muscles are affected out of proportion to other muscles. Thenar eminence muscle atrophy is the most profound finding on physical examination. Typically a patchy sensory deficit distribution along the forearm and medial arm without vascular symptoms (hand coolness or discoloration, absent pulses) is noted (44).

Numerous provocative physical examination maneuvers exist (Table 1) to produce brachial plexus impingement or irritation in disputed and true neurologic TOS and possibly PMS (5,13,14,16,17,29,32,34,35,37,39,40,42,44). All of these maneuvers will produce subjective symptoms of pain or paresthesias by the patient if positive or abnormal, and some will produce concurrent obliteration of the radial pulse (likely due to the intertwined anatomy of the brachial plexus and subclavian and axillary vascular structures). It is hypothesized that the pathophysiology of hand coolness and color changes frequently seen in NTOS during provocative maneuvers is not due to concurrent ischemia as in arterial TOS (34). Rather, brachial plexus nerve compression creates hyperreactivity of the sympathetic plexus, inducing a Raynaud phenomenon (4,34). Arguments have been raised against many of these maneuvers (3,16,26,29,44); however they remain a piece of the diagnostic evaluation process and are utilized largely as confirmatory testing for NTOS.

Table 1

Table 1

Complementary to the proposed Raynaud phenomenon with NTOS, hypoperfusion represented by hypoxia on a pulse oximetry meter during maneuvers has also been described. Compared with controls who do not have symptoms with provocative maneuvers and maintain mean pulse oximetry readings of 97% at rest and 94% during maneuvers, patients with symptoms suggestive of NTOS had a mean pulse oximetry reading of 98% at rest and 86% during maneuvers (5). Pulse oximetry may be a useful diagnostic tool, especially in clinicians seeking more objective diagnostic criteria.

Tenderness to palpation in the supraclavicular region has been described in NTOS, as well as over the anterior chest wall and scalene and trapezius muscles (26,35,44). In addition, ASM blocks by injection of a few milliliters of local anesthetic can aid the diagnosis of NTOS and may help predict a good response to surgical intervention if a patient reports subjective symptom relief (26,35,44).

In traumatic TOS, the signs vary depending upon the structure(s) injured. Brachial plexus injury presents with medial arm, forearm, and hand weakness/numbness (16,43,44). Subclavian artery injury presents with an audible bruit and/or diminished to absent distal pulses with arm elevation (16,43,44). Subclavian vein injury presents with a diffusely edematous upper extremity and ipsilateral thoracic venous dilation (16,43,44).

PMS presents commonly with tenderness to palpation along the PMM and tendon, and alleviation of symptoms after performing a pectoralis muscle block (27,32,37). The aforementioned provocative maneuvers frequently can create symptoms in patients with PMS (37,40,42), although Sanders et al. (37) found positivity more common in those patients with combined NTOS and PMS. Vemuri et al. (42) described a physical examination maneuver that may be specific to PMS, whereby there is tenderness and reproduction of symptoms to palpation over the subcoracoid space, with partial alleviation of symptoms when the patient concurrently contracts their pectoralis major muscle.

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In true NTOS, specific EDX patterns will be present and reproducible across patients (16,35,40). Consistent EDX findings remain controversial in disputed TOS (40,44). Many argue that the utility of EDX lies in its ability to confirm or rule out other pathologies to explain the patient’s symptoms (e.g., carpel tunnel syndrome or cervical radiculopathy) (31,39,40). No pathognomonic EDX findings have been delineated in PMS or traumatic TOS.

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Diagnostic imaging

Plain radiographs are useful diagnostic tests in true neurologic and traumatic TOS because they reveal the presence of cervical ribs and clavicle fractures, respectively. As discussed previously, Cho et al. (11) have shown the possible relationship between a lower positioned shoulder girdle on radiographs in NTOS. Computer tomography (CT) and magnetic resonance imaging (MRI) are felt sometimes to provide inconsistent diagnostic benefit in NTOS because CT does not provide soft tissue anatomic detail (19) and neither reliably identify fibrous bands (44). Proponents argue that MRI can identify reliably congenital bands or a well-developed scalenus minimus muscle (2,13,25) and that these modalities provide important anatomical detail about sites of compression during provocative maneuvers (2,13,14). If utilized, MRI is preferred as it provides the necessary soft tissue anatomical detail and does not require ionizing radiation (14).

Demirbag et al. report that patients with physical examination findings consistent with disputed TOS have measurable anatomical changes on MRI. Specifically their interscalene angles, angle between first rib and horizontal axis, and minimal costoclavicular distances decrease when in provocative positioning compared with neutral positioning, which did not occur for the control group (13). Parks et al. report that CT angiography is a modality that can show measurable costoclavicular space narrowing, as indicated by their evaluation of an elite archer with NTOS symptoms during draw positioning. When placed in a provocative position reproducing his draw positioning, symptoms as well as appreciable costoclavicular space narrowing was documented compared with his contralateral, unaffected side in neutral positioning (28).

Sonography with color Doppler, CT and magnetic resonance (MR) angiography and venography, arterograms, and venograms may be indicated if concurrent vascular compromise is suspected in traumatic TOS. Keep in mind that conventional arteriography and venography have been supplanted largely by the less invasive procedures of sonography, CT, and MR, which also provide concurrent surrounding anatomical detail (2,14,26,34,35,43,44).

Lastly neuromuscular sonography also has been proposed as a useful diagnostic procedure in PMS, allowing for visualization of subcoracoid space narrowing during provocative maneuvers (40). Neurovascular bundle compression and PMM deformation (whereby the PMM becomes angulated) have been visualized sonographically during shoulder hyperabduction in patients with disputed/postural TOS, which normalizes in neutral positioning and is not present in control subjects (40).

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Differential Diagnosis

The differential diagnosis of upper extremity paresthesias, myalgias, and weakness is broad (Table 2). Given the frequently absent objective criteria in NTOS and clinical presentation that can overlap with other common conditions (e.g., carpal tunnel syndrome and cervical degenerative joint disease (DJD)), special consideration of alternative pathologies are necessary (1,4,16,26,35,40,44).

Table 2

Table 2

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True neurologic and disputed TOS are treated very differently. True NTOS requires immediate surgical intervention to prevent further nerve damage. The goal of management is to arrest further hand muscle atrophy, recognizing that the level of dysfunction/atrophy at the time of presentation is likely permanent. Surgical sectioning of the congenital band is required, with the option of cervical rib resection (44). Some controversy regarding surgical approach has existed; however, the supraclavicular approach is now deemed superior to the transaxillary approach for this condition (44).

To date there are no randomized control trials comparing conservative therapies to surgical intervention in disputed TOS (30). While more studies exist on surgical management of NTOS than medical management, it is accepted generally that disputed TOS initially should be treated medically with symptom control and physical therapy (35,41,44). Clinicians should utilize multiple modalities for symptom alleviation, including rest, work restrictions, analgesics, anti-inflammatories and muscle relaxants (26,35,44). Physical therapy modalities are vast and have evolved since Peet first described TOS, including behavior modification education, ergonomics and posture modification, manual therapy, stretching exercises, biofeedback, and trigger point injections (30,35,41). It has been argued that physical therapy aimed at strengthening, resistance exercises, and neck traction worsen patient symptoms (35).

Surgical intervention for disputed TOS can be considered after failure of at least 3 months of attempted medical therapy and includes an array of modalities that excise the scalene muscles and/or first rib, with possible congenital band lysis (26,35,44). A 2010 Cochrane review article found that the only randomized prospective trial to date comparing two different surgical interventions in disputed TOS determined that the transaxillary first rib resection had better results than the supraclavicular neuroplasty of the brachial plexus (30). Rochlin et al. (31) found predictors of poor response to first rib resection and scalenectomy after failure of conservative modalities by patient-reported quality-of-life scores. These include comorbid chronic pain syndromes and active tobacco and opioid use.

Traumatic TOS management depends upon which neurovascular structures are injured. If it is solely a brachial plexus injury with mild symptoms, initial nonoperative management is appropriate (44). The presence of any vascular compromise often requires surgical intervention, for which various techniques for clavicle open reduction internal fixation and vascular repair have been described (44).

PMS has been treated successfully with physical therapy, focusing on posture correction and PMM stretching (37). For those who fail conservative treatments, pectoralis minor tenotomy (PMT) through a transaxillary incision has been described, which can be performed in the outpatient setting with local anesthesia and conscious sedation (32,37,42). Of special note, an entity termed recurrent NTOS refers to patients that have persistent symptoms after either medical or surgical intervention. Sanders et al. (32,37) argue that many of these patients have undiagnosed PMS that either existed in isolation at the time of initial evaluation or concurrently and is in many cases responsible for residual symptoms.

Other nonsurgical means of management are being explored in NTOS, like botulinum toxin injections. Utilizing the same ideas as lidocaine injection to create muscle blockade, botulinum toxin injections are postulated to provide prolonged symptom relief (17). Several studies have reported that patients experience 1 to 3 months of symptom relief when muscle injections occurred in the anterior and middle scalenes, trapezius, pectoralis minor, and subclavius (17,30). A randomized control trial comparing botulinum toxin injection to placebo (saline injection) into the ASM showed no difference in symptom control and argues for the need for more trials to be performed (17). Although botulinum toxin injection therapy seems to offer temporary pain relief at best, it may be useful in deferring surgical intervention. No studies to date have looked at repeated botulinum toxin injections for symptom relief.

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A Special Population: Pediatrics and Adolescents

Most cases of TOS of any kind occur in adulthood and are neurologic in origin (16,23,43,44). Pediatric and adolescent presentations have been referred to as “early-onset TOS.” The distribution between vascular and neurologic TOS appears to be equivalent in this population (6,9,23,26), but prevalence data are lacking due to the small number of studies that exist evaluating this population.

The etiology of TOS in pediatrics and adolescents may be narrower than their adult counterparts, with congenital anomalies and sports participation being predominant themes. Both NTOS and PMS most commonly affect pediatric and adolescent athletes, with repetitive overhead physical activities being more of a risk factor than the common motor vehicle accident-precipitated symptoms in adults (6,23,33).

NTOS and PMS treatments initially should be conservative focusing on physical therapy and cessation of sports activities prior to advocating for surgical intervention (6,33). Surgical management remains a mainstay of treatment in this population as literature to date reports good outcomes (6,23,26,33). Surgery can be catered toward the individual, utilizing PMM and scalene muscle blocks and associated symptom alleviation to guide which surgical procedure is performed (33). PMT for PMS and a combination of supraclavicular or transaxillary approaches for cervical rib resection, first rib resection, and/or scalenectomy for NTOS are being performed with good success in this population (6,9,23,33).

Although pediatric and adolescent TOS has been well described as a medical entity, delay in diagnosis often ensues due to its atypical age presentation. Given the high prevalence of athletic involvement of these patients, this medical entity must remain well known to sports medicine physicians.

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TOS represents numerous clinical entities, for which neurologic TOS (NTOS) is a main contributor. If NTOS is defined as any manifestation of brachial plexus injury, then true neurologic TOS, disputed TOS, traumatic TOS, and PMS should be considered within its spectrum. Proper diagnosis relies on patient history, physical examination findings, diagnostic testing, and possibly the utilization of EDX studies. Recognition that the disputed form of NTOS encapsulates many patients and no gold standard test exists for its diagnosis. Acknowledging that numerous sports-related activities can result in NTOS also is important.

Management options should be in most cases initially conservative, with focus on physical therapy and postural changes. For those that fail medical management, surgical options exist. Jere W. Lord (21) in 1953 insightfully wrote, “If one analyzes the anatomical structures through which the [brachial plexus,] subclavian and axillary artery and vein must pass, then it is evident that no single operative procedure can be successful in all cases of the shoulder girdle syndromes.” This has been further confirmed through the overlap between NTOS and PMS and the established results of patients sometimes requiring multiple surgical interventions for symptom alleviation (1,33,37,39,42). Few prospective randomized control trials exist comparing medical therapies to surgical interventions or contrasting different surgical techniques, making this a necessary area of future TOS research.

The authors declare no conflicts of interest and do not have any financial disclosures.

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