Current Clinical Concepts: Rehabilitation of Thoracic Outlet Syndrome

The prevalence of TOS in the general population remains unclear. Among industry and service workers including hairdressers, assembly line workers, and cash register operators, the prevalence has been reported to be 18%, with an even higher prevalence of 70% reported in computer users and musicians.¹  Secondary to challenges with diagnosing TOS, a wide range of incidence has been reported in the general population. The incidence has been reported as between 30 and 5000 per 1 million people and upward of 28 cases of neurogenic TOS and 8 cases of venous TOS per 1 million people per year.^2,10,11  Several case reports regarding all types of TOS in athletes have been published, but few researchers have studied the incidence and prevalence specifically in overhead athletes.^7,10,12–15  Otoshi et al found a prevalence of 32.8% in high school baseball players, whereas van de Pol et al found a prevalence ranging from 11% to 27% in elite volleyball players.^12,13 

The prevalence of each subcategory has been better established: around 95% for neurogenic TOS, 3% for venous TOS, and 1% for arterial TOS.¹⁶  Neurogenic and venous TOS are most common in athletes because the repetitive overhead stresses create mechanical compression due to hyperabduction and extension of the upper extremity.⁷  Neurogenic TOS in the general population is common in 20- to 50-year-old women.¹⁴  Although the reason is not completely understood, researchers have speculated that it is due to the higher incidence of cervical ribs in women.¹⁷  Venous TOS in the general population is more common for those in their 20s to 30s and more typically affects men and the dominant arm. Arterial TOS is usually due to congenital or anatomic abnormalities, making it less common in the general and athletic populations. Arterial TOS, like neurogenic TOS, is more common in women because of the greater occurrence of cervical ribs.¹¹ 

The type of TOS refers to which structure in the thoracic outlet is affected: brachial plexus, subclavian artery, or subclavian vein. The 3 potential sites of compression include the interscalene triangle, costoclavicular space, and subcoracoid space (Figure 2).¹⁸  These locations contain at least 2 neurovascular structures, so neurogenic, venous, or arterial compression can occur at these locations. The interscalene triangle comprises the anterior and middle scalene muscles and the first rib. Both the anterior and middle scalene muscles attach on the first rib, with the first rib forming the base of the interscalene triangle. The costoclavicular space comprises the subclavius muscle, the clavicle, and the first rib or anterior scalene muscle and is most easily visualized as the space between the first rib and the clavicle. This is where the subclavian vein is most vulnerable. Lastly, the brachial plexus and the axillary artery are most implicated in the subcoracoid or retropectoralis space. This space comprises the pectoralis minor muscle, ribs 2 to 4, and the coracoid process, with the pectoralis minor muscle and chest wall forming the anterior and posterior borders, respectively.^14,19,20 

Thoracic outlet syndrome involves compression and irritation of the brachial plexus as it runs through any of the aforementioned locations. Compression and irritation are usually due to repetitive injury that results in scarring and hypertrophy of the muscles surrounding the nerves, leading to scar tissue deposition on the nerves themselves. In the presence of preexisting anatomic variations, this nerve disruption can be exacerbated.⁷  Presentation varies because of the potential sites of compression combined with the location of the brachial plexus that is involved (ie, root, trunk, division, cord, branch).

Venous TOS is a chronic disease process in which repetitive insult to the subclavian vein during upper extremity elevation causes scar tissue development. The term is often used interchangeably with Paget-Schroetter syndrome (PSS).¹⁶  Although this process may be asymptomatic for years because of compensatory blood routes, it can eventually create an acute thrombus in the subclavian vein that can impede circulation. Sudden swelling, cyanosis, heaviness, pain, and early fatigue in the upper extremity often result. With PSS, the subclavian vein is compressed between the clavicle and the first rib; whereas PSS is far less common than neurogenic TOS, the incidence is higher in younger competitive athletes. Chronic overuse of the upper extremity can cause an initial injury to the subclavian vein, which initiates a cascade of fibrosis within and around the wall of the subclavian vein. This repetitive cycle leads to the fibrosis and narrowing of the subclavian vein. Like venous TOS, it is usually asymptomatic until a clot forms.¹⁵ 

Arterial TOS results from prolonged and sustained compression of the subclavian artery, commonly seen in the presence of a bony abnormality such as cervical rib or hypoplastic first rib. This compression leads to degeneration in the arterial wall and subsequent thrombus formation.

Congenital, traumatic, and a variety of functional factors such as postural positioning and repetitive stresses can contribute to the onset of TOS. Congenital causes include cervical ribs and fibrous bands, but first rib anomalies and cervical muscle variations have also been reported.^1,12,20  Cervical ribs are more commonly seen in individuals with symptomatic TOS than in asymptomatic individuals.²¹  Muscle anomalies including variable insertion sites and overlapping, extra, fused, or hypertrophied muscles are risk factors for compressing neurovascular contents.²⁰  Traumatic causes include whiplash injuries in which a rapid hyperextension-flexion moment to the neck, causing a chronic inflammatory response and compressing neurovascular structures, occurs. Other traumatic causes include first rib or clavicular fractures, falls, repetitive neck movements, and repetitive arm movements with work or sports (ie, repetitive overhead motion).¹⁹  These repetitive injury mechanisms can lead to any of the 3 types of TOS.

Specific to overhead athletes, the inherent high-velocity, repetitive overhead movements performed for their respective sports put them at risk for developing TOS. The hyperabduction and overhead positions in sports such as baseball, softball, swimming, and volleyball can disrupt the neurovascular structures. These motions can cause microtrauma in the muscle fibers, leading to hemorrhage and microscopic scar tissue within the scalene muscles and ultimately leading to muscle fibrosis. Muscle hypertrophy, which may result from or cause shoulder girdle instability, muscle imbalances, adaptive muscle shortening, or alterations in joint biomechanics, can lead to the onset of TOS. Over time, this neurovascular stress can impair blood flow, causing inflammation and fibrotic changes that can further decrease nerve compliance in an already narrowed thoracic outlet.^14,15  If overhead athletes have any control, strength, or joint restriction as the force is transferred from the lower body up the kinetic chain, the energy could dissipate, and the thorax, shoulder, and arm must make up for the lost energy.¹⁰  This can lead to instability in the cervicothoracic and scapulothoracic regions, stiffness in the scalene muscles, and other positional changes of the scapula on the thorax. Without adequate serratus anterior muscle counterforces, maladaptive first rib elevation and a depressed and downwardly rotated scapula can compress the neurovascular structures running through the thoracic outlet.¹⁰  A summary of risk factors is provided in Table 1.

Symptoms of neurogenic TOS include neck, shoulder, and arm pain at rest; paresthesias; night pain; weakness; and occipital headaches.^1,3,7,22  Pain and paresthesias are worsened with overhead movements.^1,3  Paresthesias often affect the arm and hand and do not follow peripheral or nerve root distributions, depending on the location of compression. Individuals may report a loss of grip strength or finger dexterity.^3,22  In overhead athletes, clinicians should suspect neurogenic TOS when athletes report loss of velocity and accuracy and heaviness in the arm after throwing.⁷ SOR: A

Symptoms of venous TOS include diffuse shoulder, neck, and arm pain accompanied by edema throughout the arm, cyanosis, and a subjective report of a feeling of heaviness.^3,22,23  On visual examination, the patient may have dilated collateral veins of the shoulder, chest wall, and arm.²³  Reports of nondermatomal paresthesias throughout the fingers and hand are common.²² SOR: A

Symptoms of arterial TOS include paresthesias in the fingers and hands; however, the most common concerns are coldness and cold intolerance.^3,22  Overhead movements typically worsen symptoms and can lead to pallor, pulselessness, or both in the hand.^3,22  If clinicians suspect arterial TOS, they should refer patients to a vascular surgeon for optimal management.^3,23 SOR: A

Various conditions present with symptoms like those of the TOS types referenced above; however, a hallmark of TOS is the presence of unilateral, upper extremity symptoms. A list of common differential diagnoses and their associated symptoms is provided in Table 2.

Given the complexity and systems affected by TOS, clinicians may include the Short-Form McGill Pain Questionnaire instead of a visual analog scale to assess pain.¹⁴  This questionnaire has patients localize their pain, describe their pain and its intensity, and identify the pattern of pain. Strand et al reported that the minimal clinically important difference (MCID) was a change greater than 5 points.²⁴ SOR: B

The Cervical Brachial Symptom Questionnaire is used to assess outcomes in the nonoperative and operative management of patients diagnosed with TOS.²⁵  The instrument has demonstrated high reliability (r = 0.87) and an internal consistency of 0.93 (Cronbach α); however, the MCID is unknown.²⁶ SOR: B

The Disabilities of the Arm, Shoulder and Hand has excellent test-retest reliability (r = 0.81–0.91) for patients with musculoskeletal upper extremity problems.²⁷  This instrument has been found to be responsive and is frequently used to track patient outcomes, with an MCID of 12.6 points.²⁷ SOR: B

Postural observation may reveal rounded shoulders and scapulae that are downwardly rotated, depressed, or both.²²  In advanced cases of TOS, atrophy may be detectable in the thenar and hypothenar compartments.³  Clinicians should observe the upper limb for edema, cyanosis, or pallor, which may indicate vascular TOS.²²  Palpation of the scalene triangle, subcoracoid space, or both may result in pain or reproduction of paresthesias.^3,7 SOR: C

Range of motion (ROM) of the neck and upper quarter should be assessed.^7,22  Scapular dyskinesis is commonly seen in TOS and should be evaluated. Baseball players with neurogenic TOS have been reported to have reduced external rotation and total ROM in the throwing arm compared with healthy controls.²⁸ SOR: B

Pectoralis major and minor, scalene, and upper trapezius muscles are commonly shortened and require evaluation.¹⁴  Force-production assessment should include examination of the scalene, pectoralis major and minor, rotator cuff, and accessory scapular muscles.³  We recommend measuring strength via a handgrip dynamometer or manual muscle test. Clinicians should consider using a handgrip dynamometer to assess for deficits in grip strength, as hand gripping can result in pain or parasthesias.^3,7 SOR: C

A neurologic examination should include reflex, sensation, and vibratory testing, which may be diminished.^3,7 SOR: C

Provocative testing can aid in the diagnosis of TOS. A full list of tests and their psychometric properties is provided in Table 3.²²  Balderman et al recently designed diagnostic criteria to assist in the diagnosis of neurogenic TOS.²⁹  They advocated for using the upper limb tension test (ULTT); 3-minute elevated arm stress test (EAST); and assessment involving principal symptoms, symptom characteristics, clinical history, and physical examination.^7,29  The detection of upper limb swelling and cyanosis along with positive EAST, ULTT, and Adson tests increases the likelihood of venous TOS.^22,30  The detection of upper limb ischemia, bruits, and blood pressure differential greater than 20 mm Hg along with positive EAST, ULTT, and Adson tests increases the likelihood of arterial TOS.^22,30 SOR: B

Thoracic outlet syndrome is a diagnosis of exclusion and determined with a thorough clinical examination; however, imaging can play an important role in characterizing the extent of possible compression.^30,31  Radiographs of the chest and cervical spine are used to detect bony abnormalities including cervical ribs.^30–33  Magnetic resonance imaging is used to characterize soft tissue structures contributing to compression. Results should be interpreted with caution, as the rate of venous compression is high in patients without symptoms of TOS.^30,34  Duplex ultrasound, computed tomography, or magnetic resonance imaging venography may be ordered to rule in venous TOS.^30,34  Duplex ultrasound, contrast arteriography, or finger plethysmography may be ordered to rule in arterial TOS.³⁰  The clinician may also order nerve conduction studies or needle electromyography to assist with differential diagnosis.^30,31 SOR: B

The primary rehabilitation goal is to limit tensile loads, compressive loads, or both across the thoracic outlet region when athletes return to sport (RTS) activities.³⁵  A multimodal treatment program is recommended for athletes with TOS. Summarized recommendations are provided in Table 4.

Postural abnormalities associated with TOS are due to strength and recruitment difficulties or soft tissue contracture. With soft tissue contracture, soft tissue mobilization can be used to improve static posture.³⁶  Techniques used include direct pressure, parallel deformation, or perpendicular strumming to the muscle or muscle-tendon unit.³⁶  Instrument-assisted soft tissue mobilization can be used as an adjunct to manual therapy to reduce tissue viscosity, provide myofascial release, decrease pain, and improve flexibility.³⁷  Dry needling is a form of trigger-point release used to help decrease muscle hypertonicity. The medical provider must be competent with dry-needling technique for the scalene muscles to avoid injuring nearby neurovascular structures. Dry needling as an adjunct treatment for targeting postural mobility of the latissimus dorsi and pectoralis muscles is a consideration for athletes who are not making adequate progress with standard-of-care techniques. SOR: C

Joint mobilizations can be used depending on examination findings. Common mobilization techniques include the first rib, thoracic spine, cervicothoracic junction, and lateral cervical glides.^35,38  Inferior first rib mobilizations can be used to increase the costoclavicular space and decrease compression on the neurovascular structures.³⁶  Glenohumeral joint mobilizations can be used if ROM deficits exist, as mobilizations can compress the costoclavicular space.³⁹  Posterior glenohumeral joint mobilizations are used to improve posterior capsule mobility and improve function in overhead athletes.³⁵  Thoracic spine mobilizations including posterior-anterior mobilizations can be used to decrease thoracic kyphosis and improve static posture. Secondary to cervical musculature hypertonicity associated with TOS, decreased cervical and thoracic facet-joint mobility is a common examination finding. Cervical mobilizations include lateral glides to improve facet-joint mobility. SOR: C

Pectoralis major and minor, scalene, upper trapezius, sternocleidomastoid, and latissimus dorsi muscles are all commonly shortened with TOS.¹⁴  A thorough examination is important to identify any tensile stress associated with symptoms. If tensile stress is present, lengthening shortened tissues can recreate symptoms.³⁵  An example would be pectoralis stretching completed in a door frame or over a foam roller recreating the EAST position and bringing the clavicle into the first rib, recreating symptoms.³⁵  A supine position with the arm supported is recommended to help mitigate symptoms.^35,36  Scalene muscles attach on the first rib and contribute to first rib elevation, which can compress the thoracic outlet. These muscles can be stretched using an inferior first rib mobilization with cervical spine ipsilateral rotation and contralateral side bend.³⁹  Other cervical musculature that can be stretched includes suboccipital, upper trapezius, and levator scapulae muscles secondary to their effects on posture. Other techniques such as contract-relax or other proprioceptive neuromuscular facilitation techniques can be used to help improve soft tissue mobility.³⁶  Clinical decision making based on the objective examination findings and monitoring patient response are important considerations for dosing stretching interventions. SOR: C

A cornerstone of TOS rehabilitation consists of normalizing scapular muscle recruitment. Muscles primarily requiring facilitation to improve scapular control include the middle and lower trapezius and the serratus anterior.⁴⁰  The emphasis with strengthening progressions should be placed on neutral positioning of the scapula and maintaining control against the thorax with sufficient posterior tilt of the scapula to keep the medial border stabilized.⁴⁰  Individuals with TOS typically develop fatigue earlier than healthier individuals; thus, endurance and isometric strength should be prioritized early in the rehabilitation process.⁴¹ 

A gradual progression of forces when working on scapular control is a critical rehabilitation consideration. Starting with a set/repetition scheme to challenge the athletes without use of compensatory patterns is important. A combination of isometric or light-weight, high-set/repetition schemes is recommended, gradually progressing to an isotonic and hypertrophy-oriented set/repetition scheme as scapular control progresses. Humeral-abduction angles increase the lever arm and can further challenge activation and recruitment. In previously published outlines, authors described a rehabilitation progression focusing on scapular control in ranges of abduction.^40,42  Phase 1 starts with shoulder movements below 30° of abduction, and each subsequent phase progresses shoulder movements to 90° of abduction and overhead activities.^40,42  An example of scapula-neutral strengthening progressions is outlined in Tables 5 through 10, with exercises illustrated in Figures 3 through 7. In late-stage rehabilitation, working through a sport-specific progression with scapular control to minimize symptoms is an important consideration before returning to sports. SOR: A

Blood-flow–restriction (BFR) training is an intervention used in rehabilitation for a wide variety of injuries. However, secondary to arterial TOS and venous TOS, BFR is not a recommended treatment for TOS.⁴³  From a mechanistic standpoint, BFR creates an ischemic and hypoxic muscle environment, causing high levels of metabolic stress in combination with exercise.⁴³  In a case study, Noto et al described a patient with TOS who progressed to PSS secondary to KAATSU training, a form of BFR.⁴⁴  No other literature exploring BFR as a treatment consideration for TOS exists. SOR: C

Neural glides in athletes with neurogenic TOS can be incorporated when neural mobility is decreased on clinical assessment. Neural mobilizations with TOS primarily target the median and ulnar nerves.³⁹  Caution should be exercised when using neural mobilizations to ensure they are completed in a pain-free manner and only when no tensile sensitivity is identified. SOR: C

Breathing is an important consideration in decreasing thoracic outlet compression. Accessory breathing strategies can contribute to hypertrophy of scalene, sternocleidomastoid, and trapezius muscles.⁴⁵  Athletes with neurogenic TOS often demonstrate accessory breathing strategies versus diaphragmatic breathing, potentially contributing to their symptoms.⁴⁵  Using interventions to improve diaphragmatic breathing can help to reduce thoracic outlet compression. Core stability training combined with diaphragmatic breathing can help improve carryover of breathing techniques to sport-specific activities. SOR: C

Short-term management of acute and highly irritable TOS can include external support with bracing or taping. Taping can provide additional support for the shoulder girdle and is recommended for athletes who have improved symptoms with scapula elevation.⁴⁰  Watson et al described an axillary-sling technique to help create scapular elevation and upward rotation (Figure 8).⁴⁰  Other external support or bracing includes using a pillow or towel roll under the arm to assist with lifting the shoulder girdle.³⁵ SOR: C

Local anesthetic blocks of the anterior scalene muscles provide both analgesic and muscle relaxation for symptom relief.⁴⁶  Anesthetics are used as a predictor of which athletes would benefit from decompression surgery.⁴⁶  Given the short-term relief provided by local anesthetics, they are more useful as a predictor of success with decompression than as an adjunct to rehabilitation approaches.⁴⁷ SOR: B

Botulinum toxins are neurotoxins injected to help treat focal muscle hyperactivity.⁴⁷  Researchers have hypothesized that they can help patients with neurogenic TOS secondary to their analgesic and muscle-relaxant properties.⁴⁷  Literature support has been inconsistent regarding its efficacy in patients with neurogenic TOS.¹⁶  Authors of observational studies have demonstrated varying levels of long-term success with botulinum toxins.⁴⁷  However, botulinum toxins can help athletes progress in supervised rehabilitation, with short-term results lasting up to 3 months.⁴⁸ SOR: B

Approximately 60% to 70% of athletes with neurogenic TOS have success with nonoperative management consisting of supervised rehabilitation and activity modification.⁴⁸  A 4- to 6-month trial of nonoperative management of neurogenic TOS should be completed before surgery is considered.¹⁶  Operative outcomes for neurogenic TOS have been well established, with 85% to 90% of the general population reporting symptom improvement and similar outcomes reported in the overhead athlete population.^7,15 

Often, for venous or arterial TOS, the initial line of treatment is surgical intervention. Excellent outcomes have been shown after surgical decompression for venous TOS, with most athletes returning to high levels of functional performance within an average of 3.5 months of treatment.⁷  With arterial TOS, postoperative RTS is expected by 4.7 months postintervention.⁴⁹ 

Timelines for RTS readiness vary greatly depending on symptom severity and cause. With neurogenic TOS managed nonoperatively, gradual RTS can be integrated within 4 to 6 weeks depending on rehabilitation progressions.⁵⁰  Postoperative management of neurogenic TOS has a slightly prolonged RTS timeframe. Four to 6 months postoperatively has been recommended for RTS, with athletes continuing to note improvements in strength and function for 9 months to 1 year postoperatively.⁵⁰ 

No functional testing algorithms have been previously established to determine RTS readiness in athletes with TOS. Using previously established upper extremity functional testing algorithms can help objectively determine RTS readiness.^51,52  Schwank et al discussed the importance of individualizing the RTS testing based on sport-specific demands of the individual athlete.^49,52 Table 11 provides minimum RTS considerations.⁵¹ 

Thoracic outlet syndrome is a complex constellation of symptoms and is a diagnosis of exclusion. Multidisciplinary, multimodal management is recommended to ensure optimal patient outcomes. Understanding the pathophysiology of TOS is necessary to perform a comprehensive examination. Rehabilitation is often the first line of management for patients with TOS, focusing on various manual therapies, stretching, and neuromuscular coordination exercises. The individualized physical impairments that may be causing or worsening the patient’s symptoms must be addressed.