Thoracic outlet syndrome (TOS) is a nonspecific diagnosis that refers to an array of conditions caused by compression of the neurovascular structures that pass through the thoracic outlet. Previous terms for TOS were based on the precise mechanisms or anatomic structures that caused thoracic outlet compression, including cervical rib syndrome, scalenus anticus syndrome, scalene medius syndrome, hyperabduction syndrome, costoclavicular syndrome, pectoralis minor syndrome, and first thoracic rib syndrome. Because of the variety of clinically and etiologically distinct conditions that can produce TOS, the diagnosis should specify the neurovascular structure that is compressed. The most logical TOS categories are neurogenic TOS (NTOS), venous TOS (VTOS), arterial TOS (ATOS), and mixed TOS. This review is organized to address individually the etiology, clinical presentation, diagnosis, and management of each TOS type. Table 1 provides clinical comparisons of the three types of TOS.
A PubMed MEDLINE database search was conducted on May 15, 2009, using the search term "thoracic outlet syndrome," for years "2006 to present." Overall, 170 articles were identified. Abstracts were reviewed, and all articles that involved a TOS patient series (more than two patients) undergoing specific treatments with outcomes were retrieved. Twelve studies met study criteria and were included in this review; they are summarized in Table 2. These series comprised patients with NTOS alone (1 study); VTOS patients (7 studies); NTOS and VTOS (3 studies); and NTOS, VTOS, and ATOS (1 study).
ANATOMY AND FUNCTION
The thoracic outlet, bordered by the clavicle, scapula, first rib, anterior scalene muscle, and middle scalene muscle, is the anatomic passageway for the great vessels and nerves of the upper extremity. The thoracic outlet comprises three compartments: the interscalene triangle, costoclavicular space, and retropectoralis minor space. Each compartment is a potential site of neurovascular compression.
The interscalene triangle is bounded by the first rib inferiorly, the anterior scalene muscle anteriorly, and the middle scalene muscle posteriorly. Neurovascular compression in the interscalene triangle may result from scapulary suspensory muscle injuries (e.g., cervical whiplash) and hypertrophy (e.g., repetitive overhead sports activity, such as swimming and tennis), congenital fibromuscular bands, cervical ribs, and anomalous first thoracic ribs. The costoclavicular space is formed by the clavicle and first rib. The costoclavicular space is compromised during shoulder abduction, as the S-shaped clavicle moves posteriorly. The presence of clavicular callus from previous fracture also can compress the costoclavicular space. The retropectoralis minor space stretches from the cervical spine and mediastinum to the lower border of the pectoralis minor muscle at the coracoid process. Retropectoralis minor pace volume decreases in the presence of pectoralis minor tendon hypertrophy and during shoulder hyperabduction because of conversion of the pectoralis minor tendon and coracoid into a fulcrum around which the neurovascular structures are forced to change directions.
The neurovascular structures that are compressed most frequently in TOS are the brachial plexus, axillary-subclavian vein, and subclavian artery. The brachial plexus, formed by the anterior rami of nerve roots C5 through T1, provides innervation for the upper extremity. The axillary veins pass behind the costocoracoid ligaments and pectoralis minor tendons, before advancing over the first ribs anterior to the anterior scalene muscle to join the jugular vein at the base of the neck. The subclavian arteries exit the thorax deep to the sternoclavicular joints, pass over the first ribs between the anterior and middle scalene muscle insertions, course laterally behind the clavicles where they become the axillary arteries, and then continue deep to the pectoralis minor tendons where they turn into the brachial arteries.
EVALUATION AND DIFFERENTIAL DIAGNOSIS
The evaluation of a patient with suspected TOS includes a thorough medical history, physical examination, and appropriate confirmatory diagnostic tests. The history helps direct the physical evaluation and diagnostic workup. The physical examination should include a careful evaluation of the spine, thorax, shoulder girdles, and upper extremities for range of motion, postural abnormalities, muscle atrophy, sensory loss, weakness, and areas of tenderness. Although the TOS provocative tests are of limited diagnostic value in TOS because of low sensitivities (average 72%) and specificities (average 53%), the elicitation of patient symptoms during these maneuvers may support the diagnosis of TOS (15,21,33). Table 3 lists the false positive rates for specific TOS provocative tests in asymptomatic subjects and includes the even higher rates in patients with carpal tunnel syndrome (33). The initial diagnostic study for most patients with suspected TOS is plain x-rays of the cervical spine and shoulder girdle to identify cervical ribs, anomalous first ribs, and previous clavicular trauma. Selection of appropriate advanced imaging techniques using computed tomography (CT), magnetic resonance imaging (MRI), contrast imaging, and electrodiagnostic studies should be determined by the history and physical examination.
The following conditions should be considered in the differential diagnosis of TOS: 1) shoulder joint conditions such as adhesive capsulitis, glenohumeral instability, glenohumeral or acromioclavicular osteoarthritis, rotator cuff tears, impingement, and bursitis; 2) cervical spine conditions such as spondylosis, and disc herniations; 3) neurological conditions including brachial plexus neuritis, carpal tunnel syndrome, compressive ulnar neuropathies, and complex regional pain syndrome; and 4) tumors and space-occupying lesions.
NTOS results from compression of the brachial plexus at the thoracic outlet and accounts for 95% of TOS cases (40). Women are affected twice as frequently as men, and the mean age of those requiring surgical treatment is during the fourth decade (40). NTOS may be subdivided into "true" NTOS and "disputed" NTOS. True NTOS cases have demonstrable objective physical and/or diagnostic test findings, whereas disputed TOS cases present with subjective symptoms consistent with NTOS, but lack objective characteristics. The disputed form of NTOS is far more common, comprising up to 99% of NTOS cases (40). The absence of a definitive confirmatory diagnostic test for many cases has led some to question its very existence.
Of patients with NTOS, 86% have histories of previous cervical trauma (40). Cases of true NTOS more commonly are associated with identifiable anatomic causes, such as cervical ribs, scalene abnormalities, or fibromuscular bands, but overall, only 3.9% and 0.7% of NTOS surgical patients are found to have cervical and anomalous first ribs, respectively (40). Even among NTOS patients with abnormal ribs, 80% of patients also give histories of previous cervical trauma, suggesting that abnormal ribs may only predispose to NTOS rather than represent the absolute cause (40). Scalene muscle anatomic variations also may contribute to NTOS, as a majority of NTOS surgical patients have a narrow interscalene muscle interval (13). NTOS additionally has been associated with variant scalene and levator scapulae muscles (4), as well as hypertrophied scalene anticus muscles with congenital fibrous bands (2).
The onset of NTOS symptoms usually follows hyperextension neck trauma, commonly associated with a motor vehicle accident. The traumatic event causes edema and hemorrhage within the scalene and other cervical muscles. As blood is absorbed, scar tissue forms within the muscle and around nerves, leading to upper extremity symptoms caused by muscle swelling and tightness of the scarred muscles. Histological analysis of the scalene muscles in NTOS patients demonstrates a threefold increase in muscle fibrosis (scar tissue), with muscle atrophy, and a relative loss of Type II muscle fibers (40). This mechanism is consistent with the delayed clinical presentation of TOS following cervical trauma in most patients.
In addition to upper extremity heaviness and fatigability, the clinical symptoms of NTOS are determined by the primary brachial plexus structures compressed. The "lower trunk pattern" manifests with neck and shoulder pain, paresthesias that often radiate into the medial arm, forearm, and fourth and fifth fingers, and weakness of grasp. The "upper trunk pattern" produces pain in the neck, shoulder, and face, and paresthesias that radiate into the lateral arm and simulate fifth or sixth cervical nerve root compression.
The diagnosis of "true NTOS" is established on the basis of the clinical presentation in conjunction with objective physical findings, such as weakness or atrophy of the hand, hypoesthesia of the ulnar aspect of the forearm, rib abnormalities, and abnormal electrodiagnostic testing. The diagnosis of "disputed NTOS" often is challenging, given the absence of objective physical or diagnostic test findings, and is best made by the clinical presentation, the presence of positive subjective responses to provocative maneuvers, and elimination of conditions in the differential diagnosis.
In most cases of suspected NTOS, advanced diagnostic imaging serves to narrow, rather than confirm, the diagnosis. In addition to plain x-rays, CT may provide further anatomic detail, identify scalene muscle hypertrophy, and assist in rib resection preoperative planning (6). Dynamic CT angiography with the upper extremity in hyperabduction may confirm neurovascular compression and predict a successful operative decompression (23). Cervical spine MRI is useful to disclose cervical disc disease, nerve root impingement, scalene muscle abnormalities, and compression of the brachial plexus. MRI of the brachial plexus can identify perineural pathology, as well as nerve enhancement and signal intensity differences (46). MRI and magnetic resonance (MR) angiography with the upper extremity in various anatomic positions can confirm any dynamic positions of neurovascular compression (15,28). MR neurography involves the injection of dye around the brachial plexus and is useful to display deviations in the normal course of the nerves (20). Venography is not necessary routinely in the evaluation of NTOS.
Electrodiagnostic testing (EDX), using electromyography (EMG) and nerve conduction velocities (NCV), generally has low sensitivity and specificity in the diagnosis of NTOS (40). Nonetheless, some patients with NTOS may demonstrate abnormalities in NCV, ulnar sensory nerve action potentials, compound motor action potential, and F-wave latency. EDX is perhaps most useful to uncover other neurological conditions, such as cervical nerve root radiculopathy, distal entrapment neuropathies, polyneuropathy, and motor neuron disease.
Somatosensory-evoked potentials may be positive in some cases of NTOS but are limited by a lack of specificity and the inability to localize abnormalities (40). Direct stimulation of the eighth cervical nerve has been used intraoperatively to confirm surgical success and to monitor recovery. The invasiveness of the procedure, however, limits diagnostic application to outpatients (40). Medial antebrachial cutaneous nerve conduction (MAC) assessment is able to detect subtle changes in sensory nerve transmission of a branch of the lower trunk of the brachial plexus, often missed by standard EDX (30,40). A combination of MAC and C8 nerve root stimulation tests preoperatively correlates well with the NTOS diagnosis (30).
Scalene muscle block is achieved by injecting a few milliliters of local anesthetic into the anterior scalene muscle belly (8,40). An effective block weakens the anterior scalene muscle and thus temporarily may relieve NTOS symptoms associated with neurovascular compression. Good subjective response to the scalene muscle block correlates well with a favorable surgical outcome (8). Botulinum toxin scalene muscle injection chemodenervation has been used similarly to establish the diagnosis and reduce symptoms of NTOS (27).
Recent treatment series of patients with NTOS are summarized in Table 2. Patients with NTOS should undergo at least 3 months of conservative treatment before considering surgery. Nonoperative treatment is most effective in patients who are middle-aged, female, obese, and have poor posture. Young, athletic patients may not respond so favorably (40). The cornerstone of conservative treatment involves physical therapy using gentle (e.g., the Felden-Krais method), rather than aggressive, rehabilitative exercises (9,40). Treatment adjuncts that may be applied include behavior modification, ergonomic correction, relaxation exercises, manual therapy, stretching of the neck and shoulder muscles, modalities, biofeedback, trigger point injections, muscle relaxants, nonsteroid antiinflammatory drugs (NSAID), and work restrictions. Of 50 patients who participated in a 6-month therapeutic exercise program, 94% showed clinical improvement (22); however, the study used no control group. Conservative treatment has been shown to reduce symptoms, improve function, and facilitate return to work in most patients (50). No conclusions yet have been established on which type of conservative treatment is most effective and whether it is better than placebo (50).
There are no recent, well-designed, randomized clinical trials that compare conservative and surgical therapies for NTOS. Indications for surgery are progressive neurological dysfunction, acute vascular insufficiency (associated with VTOS or ATOS), and refractory pain with functional impairment that fails to improve using conservative treatment. When surgery is required, the procedure should be tailored to the individual patient. Common surgical procedures include various combinations of first rib excision, fibrotic band lysis, and scalenectomy. Surgery through a transaxillary incision avoids transecting the scapular suspensory muscles and allows for decompression of all potential sites of thoracic outlet obstruction, except for the pectoralis minor tendon. Anterior scalenectomy alone, performed through an anterior supraclavicular incision, may be selected for patients with predominantly upper brachial plexus trunk symptoms. This procedure reduces hospitalization time, the risk of neurovascular structure damage, and blood loss. When comparing surgical treatment of NTOS and VTOS patients with first rib resection plus scalenectomy, NTOS patients generally recover more slowly and are more likely to require secondary procedures (11). Nevertheless, many NTOS patients respond favorably to surgery, even in the absence of preoperative objective abnormalities (40).
Upper-extremity venous thrombosis (UEDVT) of the axillary-subclavian veins is relatively uncommon, with an incidence of two cases per 100,000 person-years (26). UEDVT accounts for only 3% of all cases of deep venous thrombosis (44) and may be classified as "primary" or "secondary." Primary UEDVT includes idiopathic and activity-related cases, whereas secondary UEDVT may result from in-dwelling venous catheters, thrombophilic disorders, or underlying malignancies. The 3-month mortality rate for UEDVT is 30%; however, this includes cases with comorbid conditions, such as malignancies (25).
Activity-related or "effort thrombosis" UEDVT also is known as the Paget-Schröetter Syndrome (PSS). PSS results from compression of the axillary-subclavian veins within the thoracic outlet. Overhead-sport athletes may develop PSS from repetitive shoulder hyperabduction and external rotation that may compress the axillary-subclavian veins, cause cumulative damage to the venous intima linings, and transiently restrict venous flow. Recurring venous injury and stasis creates an environment that is conducive to the creation of thrombus.
Cervical spine extension and drooping of the shoulders predispose patients to PSS by narrowing the costoclavicular space. Anomalous insertion of the costoclavicular ligament on the first rib and hypertrophy of the scalenus muscle also are both associated with PSS (49). Thrombophilic conditions and temporary exercise-related elevation of coagulation factors additionally may lead to PSS (44). Subclavian vein obstruction also may occur as it passes deep to the pectoralis minor tendon and in association with an aberrant subclavian artery (34,40).
PSS often affects young, healthy individuals. Unlike NTOS, PSS affects men twice as frequently as women (26). Seventy-five percent of PSS patients report antecedent trauma or strenuous repetitive overhead activity within 24 h of presentation. A common clinical presentation is acute swelling of the dominantly involved upper extremity, with heaviness, effort-dependent pain, paresthesias, venous distension, and possibly visible superficial venous collaterals around the shoulder (49). PSS has been reported in baseball players (28,31,43), football players (45), ballet dancers (42), tennis players (31), swimmers (31), rugby players (38), and a hiker wearing a backpack (42). A recent systematic review of studies examining postthrombotic syndrome (PTS) after UEDVT found the mean risk for pulmonary embolus is 15% (18). Residual thrombosis and axillary-subclavian DVT additionally are associated with PTS (18).
The diagnosis of VTOS is established by the clinical presentation, physical examination, and appropriate confirmatory diagnostic studies. More than one diagnostic test method often is required (44). Venous duplex ultrasonography largely has replaced conventional venography as the initial diagnostic study of choice for suspected VTOS. Ultrasonography provides a noninvasive means to identify the presence, location, and extent of a venous thrombus (5,44). Diagnostic sensitivities range from 71% to 94% when using color duplex imaging (33,44). Nonetheless, contrast venography remains more reliable than ultrasonography (7) and routinely should be performed if a patient presents with arm swelling and cyanosis, even if the ultrasound examination is negative. If the venogram is negative with the upper extremity at the side, it should be repeated with the arm at 90° and 180° of abduction. CT and MRI venography provide outstanding detail of thrombus characteristics and the sites of external venous compression (40,47). A significant number of UEDVT patients have hypercoagulable disorders (10,24); thus, the diagnostic workup also should include obtaining routine clotting parameters (44). D-dimer levels have not been useful for risk stratification in VTOS cases (44).
No recent randomized clinical trials have been performed to determine the optimal treatment of PSS. The fact that UEDVT can embolize to the lungs reinforces the importance of making a prompt, accurate diagnosis and initiating definitive early treatment to avoid long-term complications. Recent VTOS patient treatment series are summarized in Table 2. The traditional conservative treatment of PSS consists of rest, extremity elevation, and long-term anticoagulation (1,38,49). However, because of high recurrence rates and residual symptoms, more aggressive treatment is recommended. This focuses on achieving venous patency using thrombolytics, possible stent placement, anticoagulation, and the eventual surgical decompression of the axillo-subclavian venous system (1,32,44).
For clinically apparent UEDVT, even in the presence of a normal venous duplex ultrasound examination, anticoagulation should be initiated (44). Once the diagnosis of UEDVT is confirmed, direct thrombolysis should be administered. Early thrombolysis has been shown to improve recanalization rates, compared with anticoagulation alone and is most successful if undertaken within one week of the presentation (16). Adjunctive percutaneous mechanical thrombectomy may be considered; however, there is limited evidence to support its routine use (41). Postthrombolysis percutaneous venous grafts and venoplasty, with or without stenting, may be considered for persistent venous stenosis. Stenting should be used cautiously in the presence of extrinsic compression, as it may carry an increased risk of early occlusion and stent fracture (35,48).
Thoracic outlet surgical decompression routinely is recommended for cases with residual venous stenosis or in the presence of demonstrable extrinsic venous compression (44). Surgical procedures should address the structures that externally compress the affected veins, and most techniques involve first rib resection and scalene muscle release. The timing of surgical decompression is controversial, with some experts recommending prompt surgical decompression (32,49) and others advocating that surgery be delayed to help optimize patient selection and avoid unnecessary procedures (44).
Several investigators report good to excellent PSS treatment results using combinations of thrombolysis, first rib resection, scalenectomy, subclavius muscle release, venoplasty, stenting, and anticoagulation (3,11,14,15,18,29,31,37,40,49). Individualized treatment algorithms have led to success rates from 83% to 100% (15,17,31,49). Patients typically return to unrestricted use of the affected upper extremities and competitive athletics at a mean interval of 3.5 months after surgery (31). The literature indicates that patients with PSS who present early for treatment (<14 d from the onset of symptoms) are best treated with thrombolysis and thoracic outlet surgical decompression, whereas chronic cases should be treated with surgical decompression alone (15,17). The need for venous reconstruction is best determined by the identification of residual findings after thrombolysis (15,17).
A recent PSS treatment protocol consisting of catheter-directed thrombolysis, a short period of anticoagulation, and surgical thoracic outlet decompression only for those selective patients who develop persistent or recurrent symptoms, was designed to reduce the number of PSS surgeries (28). Forty-five percent of patients required first-rib resections within the first 3 months because of persistence or recurrence of symptoms, and 93% of these had successful outcomes. Of the remainder of patients who were treated initially with thrombolysis alone (no surgical decompression), 23% experienced recurrent thrombotic events, at a mean interval of 13 months. These patients underwent subsequent first rib resections, with a 100% success rate, at a mean follow-up of 55 months (29). Stent placement and younger age both were associated with higher risks of rethrombosis (29). The optimal management of a chronically occluded subclavian vein is controversial, although first-rib resection with scalenectomy, followed by anticoagulation, often has resulted in the spontaneous opening of numerous occluded veins (14,15).
ATOS is the least common form of TOS, representing fewer than 1% of cases. ATOS results from subclavian artery compression usually caused by a cervical or anomalous first rib, scalene muscle, fibromuscular bands, or pectoralis minor tendon (42). Chronic arterial compression may lead to poststenotic arterial dilatation, aneurysm formation, thrombus development, and possible eventual distal embolization. Unlike other forms of TOS, abnormal ribs are common in ATOS, affecting 74%-100% of surgical cases (36,40). The humeral head becomes a fulcrum during the cocking phase of throwing, over which the distal one third of the axillary artery and its circumflex branches may become compressed, leading to arterial damage, activity-related claudication symptoms, and thrombus formation (36). Clavicular deformities and hypertrophic callus from previous trauma also may lead to arterial damage and predispose to thrombosis and embolization (36).
ATOS often remains asymptomatic until embolization occurs. Signs and symptoms are pain, paresthesias, cyanosis, early fatigability, coldness, and color changes of the hands and fingers because of arterial obstruction. Digital gangrene may occur. Neck and shoulder pain symptoms are less common than in VTOS and NTOS. Physical examination findings may reveal an absence of distal upper extremity pulses at rest, delayed capillary refill, and signs of ischemia of the distal fingers. Additional possible physical findings are a tender bony supraclavicular prominence, palpable pulsation of the supraclavicular artery, and an audible supraclavicular bruit when the arm is placed in a position of arterial compression.
The diagnosis of ATOS is dependent on the confirmation of arterial circulatory compromise and supported further by the identification of structural factors predisposing to arterial obstruction. The overhand exercise test, performed by having the patient raise both arms overhead and rapidly flex and extend the fingers, is a provocative test that suggests arterial insufficiency. A positive test is indicated if the patient experiences heaviness, fatigue, numbness, tingling, skin blanching, or discoloration within 20 s. As noted previously, the standard TOS provocative tests have low diagnostic values for ATOS (32)
Doppler ultrasonography, conventional arteriography, and CT or MR angiography in association with postural maneuvers are the standard studies used to identify ATOS-related dynamic circulatory compromise, arterial dilatation, and aneurysms. A recent systemic review found that the current evidence for the use of MR angiography in the diagnosis of ATOS is weak, largely because of poor existing study designs (19). Arteriography is useful in the planning of operative strategy (7,40) and has higher sensitivity when performed in the sitting rather than supine position and with different arm positions (12).
The goal of ATOS treatment is the restoration of distal arterial blood flow. Successful treatment is dependent upon the accurate identification of the site(s) of arterial compression. Surgical management options include cervical or anomalous first rib resections, scalene or pectoralis minor muscle releases, and subclavian arterial reconstructions with grafting, if indicated. Among 34 ATOS surgical patients, 22 had generally favorable outcomes when treated with cervical or anomalous first rib resections (17). Unfortunately, not all patients were able to return to their previous levels of physical activity (17). Delays in treatment for symptomatic ATOS may lead to a sympathetically maintained chronic-pain syndrome (49).
Skeletal immaturity presents a unique aspect of the surgical treatment of TOS in adolescent and teenaged patients (37). In a series of 18 young (range: 13-19 yr) TOS patients treated with first-rib resections, female patients comprised 72% of all patients, 85% of NTOS patients, and only 20% of PSS patients. The authors reported no significant operative complications and found that the treatment of NTOS in younger patients usually requires extensive surgical decompression using first-rib resection and scalenectomy. PSS also responded well to standard thrombolysis and surgical decompression, and all patients were able to return to school and competitive athletics (37). A second series of adolescents treated surgically for TOS described a similarly high relative proportion of female patients and found that 24% had "effort thrombosis"-related symptoms, 12% had hypercoagulable disorders, and vascular TOS types occurred more commonly in younger patients compared with adults (3).
Effective management of TOS requires the precise identification of the neurovascular structure that is compressed. A careful history and physical examination often will lead to the most likely diagnosis. The clinical presentations of VTOS and ATOS frequently are explicit with signs and symptoms of venous (e.g., upper-extremity heaviness and swelling) or arterial (e.g., effort-related claudication and signs of distal embolization) obstruction. Vascular ultrasonography and contrast radiography regularly confirm these diagnoses. NTOS presents the greatest challenge to the clinician as it typically lacks a definitive confirmatory imaging or diagnostic technique. TOS optimally is treated using a multidisciplinary approach that includes the sports medicine specialist, orthopedic surgeons, vascular surgeons, thoracic surgeons, cardiologists, physical therapists, and interventional radiologists. Definitive treatment of TOS necessitates the correction of any anatomical predisposing factors.
Not all cases present in classic form. This author evaluated a collegiate baseball pitcher who presented with the chief complaint of "recurrent cellulitis" of his dominant upper extremity. This cellulitis had recurred repeatedly during the previous month, and skin erythema and swelling was exacerbated following pitching outings. His coach had noticed a decline in his pitching velocity during the few months before his presentation. Examination revealed diffuse upper extremity edema with collateral superficial veins visible at the shoulder, consistent with subacute PSS, confirmed with arteriography. The athlete was treated initially with thrombolysis, anticoagulation, and surgical decompression of thoracic outlet. Unfortunately, he experienced recurrent thrombotic episodes - likely a result of the duration of symptoms - and eventually required venoplasty with grafting. His return to baseball pitching seems unlikely.
TOS is best categorized as neurogenic, venous, or arterial, based on the neurovascular structure compressed. NTOS, the most common form, usually is associated with previous cervical trauma and occasionally with cervical or anomalous first ribs and fibromuscular bands. The diagnosis of NTOS may be challenging given the frequent absence of objective physical or diagnostic test findings. Although there are no well-designed, randomized clinical trials that compare conservative and surgical therapies for NTOS, common surgical procedures include first-rib excision, fibrotic bands lysis, and scalenectomy. The diagnosis of PSS usually is established with ultrasonography and contrast venography. The treatment of acute PSS involves immediate thrombolysis and anticoagulation, with possible surgical decompression of the thoracic outlet. ATOS, the least common form of TOS, often is associated with an abnormal rib compressing the subclavian artery. The surgical management options for ATOS include cervical or anomalous first-rib resection, scalene or pectoralis minor muscle release, and subclavian arterial reconstruction.
1. AbuRahma AF, Robinson PA. Effort subclavian thrombosis: evolution of management. J. Endovasc. Ther
. 2000; 7:302-8.
2. Almeida DF, Meyer RD, Oh SJ. True neurogenic thoracic outlet syndrome in a competitive swimmer: a case report of this rare association. Arq. Neuropsiquiatr
. 2007; 65:1245-8.
3. Arthur LG, Teich S, Hogan M, Caniano DA, Smead W. Pediatric thoracic outlet syndrome: a disorder with serious vascular complications. J. Pediatr. Surg
. 2008; 43:1089-94.
4. Aydog ST, Ozcakar L, Demiryurek D, Bayramoglu A, Yorubulut M. An intervening thoracic outlet syndrome in a gymnast with levator claviculare muscle. Clin. J. Sports Med
. 2007; 17:323-5.
5. Baarslag H, van Beek EJ, Koopman MM, Reekers JA. Prospective study of colour duplex ultrasonography compared with contrast venography in patients suspected of having deep venous thrombosis of the upper extremities. Ann. Intern. Med
. 2002; 136:865-72.
6. Baltopoulos P, Tsintzos C, Prionas G, Tsironi M. Exercise-induced scalenus syndrome. Am. J. Sports Med
. 2008; 36:369-74.
7. Brantigan CO, Roos DB. Diagnosing thoracic outlet syndrome. Hand Clin
. 2004; 20:27-36.
8. Braun RM, Sahadevan DC, Feinstein J. Confirmatory needle placement technique for scalene muscle block in the diagnosis of thoracic outlet syndrome. Tech. Hand Up. Extrem. Surg
. 2006; 10:173-6.
9. Buchanan PA, Ulrich BD. The Feldenkrais method: a dynamic approach to changing motor behavior. Res. Q. Exerc. Sport
. 2003; 74:116-26.
10. Cassada DC, Lipscomb AL, Stevens SL, et al
. The importance of thrombophilia in the treatment of Paget-Schröetter syndrome. Ann. Vasc. Surg
. 2006; 20:596-601.
11. Chang DC, Rotellini-Coltvet LA, Mukherjee D, De Leon R, Freischlag JA. Surgical intervention for thoracic outlet syndrome improves patient's quality of life. J. Vasc. Surg
. 2009; 49:630-5.
12. Cornelis F, Zuazo I, Bonnefoy O, et al
. Diagnosis of thoracic outlet syndrome. Value of angiography in the sitting position. J. Radiol
. 2008; 89:47-52.
13. Crotti FM, Carai A, Carai M, Sgaramella E, Sias W. Post-traumatic thoracic outlet syndrome (TOS). Acta. Neurochir. Suppl
. 2005; 92:13-5.
14. DeLeón R, Chang DC, Busse C, Call D, Freischlag JA. First rib resection and scalenectomy for chronically occluded subclavian veins: what does it really do? Ann. Vasc. Surg
. 2008; 22:395-401.
15. DeLeón RA, Chang DC, Hassoun HT, et al
. Multiple treatment algorithms for successful outcomes in venous thoracic outlet syndrome. Surgery
. 2009; 145:500-7.
16. Divi V, Proctor MC, Axelrod DA, Greenfield LJ. Thoracic outlet decompression for subclavian vein thrombosis: experience in 71 patients. Arch. Surg
. 2005; 140:54-7.
17. Doyle A, Wolford HY, Davies MG, et al
. Management of effort thrombosis of the subclavian vein: today's treatment. Ann. Vasc. Surg
. 2007; 21:723-9.
18. Elman EE, Kahn SR. The post-thrombotic syndrome after upper extremity deep venous thrombosis in adults: a systemic review. Thromb. Res
. 2006; 117:609-14.
19. Estilaei SK, Byl NN. An evidence-based review of magnetic resonance angiography for diagnosing arterial thoracic outlet syndrome. J. Hand Ther
. 2006; 19:410-9.
20. Filler AG, Maravilla KR, Tsuruda JS. MR neurography and muscle MR imaging for image diagnosis of disorders affecting the peripheral nerves and musculature. Neurol. Clin
. 2004; 22:643-82.
21. Gillard J, Perez-Cousin M, Hachulia E, et al
. Diagnosing thoracic outlet syndrome: contribution of provocative tests, ultrasonography, electrophysiology, and helical computed tomography in 48 patients. Joint Bone Spine
. 2001; 68:416-24.
22. Hanif S, Tassadaq N, Rathmore MF, et al
. Role of therapeutic exercises in neurogenic thoracic outlet syndrome. J. Ayub. Med. Coll. Abottabad
. 2007; 19:85-8.
23. Hasanadka R, Towne JB, Seabrook GR, et al
. Computed tomography angiography to evaluate thoracic outlet neurovascular compression. Vasc. Endovascular Surg
. 2007; 41:316-21.
24. Hendler MF, Meschengieser SS, Blanco AN, et al
. Primary upper-extremity deep vein thrombosis: high prevalence of thrombophilic defects. Am. J. Hematol
. 2004; 76:330-7.
25. Hingorani A, Ascher E, Markevich N, et al
. Risk factors for mortality in patients with upper extremity and internal jugular deep venous thrombosis. J. Vasc. Surg
. 2005; 41:476-8.
26. Hurley WL, Comins SA, Green RM, Canizzaro J. A traumatic subclavian vein thrombosis in a college baseball player: a case report. J. Athl. Train
. 2006; 41:198-200.
27. Jordan SE, Ahn SS, Gelabert HA. Combining ultrasonography and electromyography for botulinum chemodenervation treatment of thoracic outlet syndrome: comparison with fluoroscopy and electromyography guidance. Pain Phys
. 2007; 10:541-6.
28. Kim S, Choi JY, Huh YM, et al
. Role of magnetic resonance imaging in entrapment and compressive neuropathy-what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image: part 2. Upper extremity. Eur. Radiol
. 2007; 17:509-22.
29. Lee JT, Karwowski JK, Harris EJ, Haukoos JS, Olcott C. Long-term thrombotic recurrence after nonoperative management of Paget-Schröetter syndrome. J. Vasc. Surg
. 2006; 43:1236-43.
30. Machanic BI, Sanders RJ. Medial antebrachial cutaneous nerve measurements to diagnose neurogenic thoracic outlet syndrome. Ann. Vasc. Surg
. 2008; 22:248-54.
31. Melby SJ, Vedantham S, Narra VR, et al
. Comprehensive surgical management of the competitive athlete with effort thrombosis of the subclavian vein (Paget-Schröetter syndrome). J. Vasc. Surg
. 2008; 47:809-20.
32. Molina JE, Hunter DW, Dietz CA. Paget-Schröetter syndrome treated with thrombolytics and immediate surgery. J. Vasc. Surg
. 2007; 45:328-34.
33. Nord KM, Kapoor P, Fisher J, et al
. False positive rate of thoracic outlet syndrome diagnostic maneuvers. Electromyog. Clin. Neurophysiol
. 2008; 48:67-74.
34. Özçakar L, Kaymak B, Turan S, et al
. Thoracic outlet syndrome, Paget-Schröetter syndrome and aberrant subclavian artery in a young man. Joint Bone Spine
. 2006; 73:469-71.
35. Phipp LH, Scott DJ, Kessel D, Robertson I. Subclavian stents and stent-grafts: cause for concern? J. Endovasc. Surg
. 1999; 6:223-6.
36. Reeser JC. Diagnosis and management of vascular injuries in the shoulder girdle of the overhead athlete. Curr. Sports Med. Rep
. 2007; 6:322-7.
37. Rigberg DA, Gelabert H. The management of thoracic outlet syndrome in teenaged patients. Ann. Vasc. Surg
. 2009; 23:335-40.
38. Roche-Nagle G, Ryan R, Barry M, Brophy D. Effort thrombosis of the upper extremity in a young sportsman: Paget-Schröetter syndrome. Br. J. Sports Med
. 2007; 41:540-1.
39. Sabeti S, Schillinger M, Mlekusch W, et al
. Treatment of subclavian-axillary vein thrombosis: long-term outcome of anticoagulation versus systemic thrombolysis. Thromb. Res.
. 2002; 108:279-85.
40. Sanders RJ, Hammond SH, Rao NM. Diagnosis of thoracic outlet syndrome. J. Vasc. Surg
. 2007; 46:601-4.
41. Schneider DB, Dimuzio PJ, Martin ND, et al
. Combination treatment of venous thoracic outlet syndrome: open surgical decompression and intraoperative angioplasty. J. Vasc. Surg
. 2005; 40:599-603.
42. Schön N, Netzch C, Kröger K. Subclavian vein thrombosis and backpacking. Clin. Res. Cardiol
. 2007; 96:42-44.
43. Simovitch RW, Bal GK, Basamania CJ. Thoracic outlet syndrome in a competitive baseball player secondary to the anomalous insertion of an atrophic pectoralis minor muscle. Am. J. Sports Med
. 2006; 34:1016-19.
44. Smith RA, Dimitri SK. Diagnosis and management of subclavian vein thrombosis: three case reports and review of literature. Angiology
. 2008; 59:100-6.
45. Snead D, Marberry KM, Rowdon G. Unique treatment regimen for effort thrombosis in the nondominant extremity of an overhead athlete: a case report. J. Athl. Train
. 2009; 44:94-7.
46. Sureka J, Cherian RA, Alexander M, Thomas BP. MRI of brachial plexopathies. Clin. Radiol
. 2009; 64:208-18.
47. Tanju S, Sancak T, Dusunceli E, et al
. direct contrast-enhanced 3D MR venography evaluation of upper extremity deep venous system. Diagn. Interv. Radiol
. 2006; 12:74-9.
48. Urschel HC, Patel AN. Paget-Schröetter syndrome therapy: failure of intravenous stents. Ann. Thor. Surg
. 2003; 75:1693-6.
49. Urschel HC, Patel AN. Surgery remains the most effective treatment for Paget-Schröetter syndrome: 50 years' experience. Ann. Thor. Surg
. 2008; 86:254-60.
50. Vanti C, Natalini L, Romeo A, Tosarelli D, Pilllastrini P. Conservative treatment of thoracic outlet syndrome: a review of the literature. Eura. Medicophys
. 2007; 43:55-70.