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Thoracic Outlet Syndrome (TOS)

Introduction

The term ‘thoracic outlet syndrome’ (TOS) refers to the compression of the neurovascular structures, primarily the brachial plexus, subclavian artery, and the subclavian vein, as they exit through the thoracic outlet also known as the cervicothoracobrachial region.

Anatomically, the thoracic outlet is bordered anteriorly by the anterior scalene muscle, posteriorly by the middle scalene , and inferiorly by the first rib .[1] [2]This area serves as a passageway for nerves and blood vessels travelling from the neck to the arm.

TOS is considered as one of the most controversial topics in musculoskeletal medicine and rehabilitation, partly due to its complex presentation and challenges in diagnosis[3].

The term ‘TOS’ does not identify the specific structure being compressed. Clinically it is typically divided into two main categories:

  • Vascular TOS, which may involve compression of the subclavian artery or vein and generally presents with fewer diagnostic problems.
  • Neurogenic TOS which involves compression of the brachial plexus and accounts for more than 90% of all TOS cases.[4]

To improve diagnostic clarity, TOS should be classified as arterial TOS (ATOS), venous TOS (VTOS), or neurogenic (NTOS), depending on the structure affected.[1][2]

Clinically Relevant Anatomy

The thoracic outlet consists of three main passageways through which neurovascular structures travel from the neck to the upper limb. Compression at any of these sites can contribute to thoracic outlet syndrome (TOS).

Interscalene Triangle

The first narrowing area is the most proximal and is named the interscalene triangle: This triangle is bordered by:

  • Anteriorly by the anterior scalene muscle
  • Posteriorly by the middle scalene muscle
  • Inferiorly by the first rib

The brachial plexus and subclavian artery pass through this space. Anatomical variations, such as the presence of the scalene minimus muscle or overlapping insertion of the anterior and middle scalenes on the first rib, can reduce the available space and contribute to compression.

Costoclavicular Space

The second passageway is called the costoclavicular space (or triangle), and is bordered

  • Superiorly by the middle third of the clavicle
  • Inferiorly by the first rib
  • Posteriorly and medially by the costoclavicular ligament

The subclavian vein, subclavian artery, and brachial plexus pass through this space. Compression of these structures can occur as a result of congenital abnormalities, trauma to the first rib or clavicle fractures. Structural changes in the subclavian muscle or the costocoracoid ligament can also be contributing factors.

Subcoracoid (Sub-Pectoralis Minor) Space

The final passage lies beneath the coracoid process, just under the tendon of pectoralis minor. It is bordered:

  • Superiorly by the coracoid process
  • Anteriorly by the pectoralis minor muscle
  • Posteriorly by ribs 2-4 posteriorly.


Shortening or tightness of the Pectoralis Major can lead to narrowing of this space, particularly during hyperabduction, resulting in neurovascular compression. [1][2][5]

Anatomical Variants and Contributing Factors

Several congenital or acquired anatomical abnormalities can further compromise the thoracic outlet, including:

  • The presence of a cervical rib
  • Congenital soft tissue abnormalities
  • Long C7 transverse process
  • Fibrous bands or muscular anomalies (e.g. a broad scalene attachment or hypertrophied scalenes)
  • Clavicular hypomobility [3]
  • Scoliosis or elevated scapula
  • Functionally acquired anatomical changes[1]. 

Soft tissue abnormalities may create compression or tension loading of the neurovascular structures found within the thoracic outlet (such as hypertrophy, a broader middle scalene attachment on the 1st rib, or fibrous bands that increase stiffness).

Epidemiology/Aetiology

TOS is a relatively uncommon condition, and its true prevalence in the general population is difficult to determine due to variations in diagnostic criteria and underreporting. However, studies suggest that it may affect approximately 3 to 80 individuals per 1,000 people, depending on the population studied and the criteria used for diagnosis [6].

It is more commonly diagnosed in women than in men, with a female-to-male ratio ranging from 3:1 to 4:1. This is thought to be influenced by anatomical and physiological differences such as narrower thoracic outlets, less-developed musculature, greater breast tissue leading to shoulder depression, and a lower anatomical position of the sternum, which may alter the angle between the scalene muscles and predispose women to compression syndrome [1][7]

The condition is most often diagnosed between the ages of 20 and 50 and is rarely seen in children [1]. Of all TOS cases, approximately 95% are neurogenic, affecting the brachial plexus, while the remaining 5% are vascular, involving either the subclavian artery or vein [4].


A variety of congenital, acquired, and muscular factors may contribute to the development of TOS. One such anatomical variation is the cervical rib, which is present in approximately 1% of the population. Of those with cervical ribs, approximately 50% have bilateral involvement [8]. Cervical ribs are often asymptomatic, but when symptomatic, they are commonly associated with neurogenic TOS, particularly when fibromuscular bands are also present [9].

Athletes who frequently engage in overhead activities, such as baseball and football players, swimmers, divers, and weightlifters, frequently expose their subclavian vessels and brachial plexuses to repetitive stress. This repetitive trauma can lead to various complications, including venous effort thrombosis, arterial occlusions, and brachial plexopathy. Among this demographic, there is a heightened susceptibility to Paget-Schroetter syndrome, also known as effort thrombosis. However, neurogenic thoracic outlet syndrome (nTOS) remains the primary manifestation of the condition across all groups.[10]

A range of anatomical and biomechanical variations may contribute to the development of TOS. These include congenital anomalies such as cervical ribs and fibrous bands, which are more likely to be associated with symptomatic cases, particularly in the presence of repetitive overhead activity or trauma [8] [9]. Further detail on contributing structures and anatomical spaces can be found in the Clinically Relevant Anatomy section above.

Clinical Presentation

The clinical presentation of TOS can vary widely depending on the type of structure affected — whether neural or vascular — and the severity of compression. Symptoms often develop gradually and may be intermittent, making early diagnosis challenging [1][3].

Neurogenic TOS (nTOS), the most common form, typically presents with sensory disturbances such as pain, numbness, tingling, and paraesthesia in the upper limb. These symptoms often involve the neck, shoulder, arm, and hand, and may follow a non-dermatomal pattern. Some patients report a sensation of heaviness, fatigue, or weakness in the affected limb, particularly during overhead activities [11]. Discolouration, temperature changes, and swelling are less common in nTOS but may occur due to secondary vascular involvement.

Symptoms tend to worsen with specific postures or repetitive movements, especially arm abduction and external rotation or sustained overhead activity. Activities such as throwing, serving in tennis, painting, driving, or typing may provoke or aggravate symptoms [3][7]. When compression involves the upper brachial plexus (C5–C7), patients may experience symptoms radiating from the neck to the ear, face, anterior chest, or lateral arm. Lower plexus involvement (C8–T1) typically results in symptoms affecting the medial forearm, ring finger, and small finger [3].

Vascular TOS is less common and typically more acute in presentation. Venous TOS may present with limb swelling, cyanosis, or a feeling of heaviness, while arterial TOS can lead to pallor, cold sensitivity, diminished pulses, or even digital ischaemia [10]. Claudication and paraesthesia may also be reported in arterial cases, especially after exertion.

Some clinicians describe patients as either “Compressors” or “Releasers”:

Compressors tend to experience symptoms during the day, especially with poor posture (e.g. forward head, protracted shoulder girdle) or repetitive activity. These patients often show symptoms while working at a desk, carrying loads, or using their arms overhead.

Releasers, by contrast, report symptoms predominantly at night. These symptoms are thought to arise from a sudden release of pressure restoring blood flow and nerve conduction, leading to paraesthesia or discomfort that may disturb sleep. This pattern may also be associated with a favourable prognosis [11][4].

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Because of its varied presentation and overlap with other upper limb and cervical conditions, TOS can be misdiagnosed or overlooked. Clinical assessment should include a detailed history and examination focused on symptom behaviour, aggravating factors, and posture-related triggers.

Type Common Patient Profile Key Signs and Symptoms
Arterial TOS (ATOS) Young adult with vigorous arm activity
  • Pain in the hand
  • Claudication
  • Pallor
  • Cold intolerance
  • Paresthesia
  • Symptoms typically appear spontaneously
Venous TOS (VTOS) Younger men involved in strenuous upper limb use
  • Cyanosis
  • Feeling of heaviness
  • Paresthesia in fingers/hand (due to oedema)
  • Arm swelling (oedema)
True Neurogenic TOS History of trauma (e.g. whiplash)
  • Pain, numbness, paresthesia, and/or weakness
  • Occipital headaches
  • Day/night symptoms
  • Loss of fine motor skills
  • Cold intolerance (possible Raynaud’s)
  • Objective weakness
  • Often identified as “Compressors” (s/s > daytime)
Disputed Neurogenic TOS Often history of trauma or posture-related onset
  • Pain, paresthesia, and subjective weakness
  • Occipital headaches
  • Nocturnal paraesthesias (frequently waking the patient)
  • Loss of fine motor skills
  • Cold intolerance (possible Raynaud’s)
  • Typically “Releasers” (s/s > night-time)

Differential Diagnosis

The symptoms of TOS can overlap with a variety of other conditions affecting the cervical spine, shoulder, upper limb, and vascular or neurological systems. Several conditions may coexist with TOS, either masking or exacerbating symptoms. These overlapping pathologies should be identified and treated independently where necessary. A thorough history and clinical examination are essential to differentiate TOS from these conditions and ensure accurate diagnosis, here are some conditions that may mimic similar symptoms[1][3][11] :

Neurological and Entrapment Syndromes

  • Cervical radiculopathy – Nerve root compression causing dermatomal pain, weakness, and sensory changes.
  • Nerve root compression (discogenic or spondylotic) – Often due to disc herniation or degeneration, mimicking neurogenic symptoms.
  • Carpal tunnel syndrome – Median nerve entrapment at the wrist causing numbness in the thumb and fingers.
  • Cubital tunnel syndrome – Ulnar nerve compression at the elbow, resulting in tingling or weakness in the ring and little fingers.
  • Radial tunnel syndrome – Entrapment of the radial nerve causing pain over the lateral forearm.
  • Brachial plexus trauma – Nerve injury from trauma, often acute and with a known mechanism.
  • Parsonage-Turner syndrome – Sudden onset of shoulder pain followed by muscle weakness and wasting.
  • Radiation-induced brachial plexopathy – Late complication of radiotherapy presenting with progressive weakness or sensory loss.
  • Complex regional pain syndrome (CRPS I and II) – Chronic regional pain with autonomic and sensory abnormalities.
  • Sympathetic-mediated pain – Neuropathic pain due to sympathetic overactivity.
  • Thoracic (T4) syndrome – Upper thoracic dysfunction with diffuse arm pain, paraesthesia, and autonomic symptoms.
  • Horner’s syndrome – Ptosis, miosis, and anhidrosis due to sympathetic disruption, sometimes indicating a serious underlying pathology.

Musculoskeletal Disorders

Vascular Conditions

  • Paget-Schroetter syndrome – Effort thrombosis of the subclavian vein, often seen in athletes.
  • Upper extremity deep vein thrombosis (UEDVT) – Venous obstruction presenting with swelling, heaviness, and cyanosis.
  • Raynaud’s phenomenon – Vasospasm in fingers triggered by cold or stress, leading to colour changes and numbness.
  • Vasculitis – Inflammatory condition of blood vessels that may mimic vascular TOS.
  • Arterial TOS – Compression of the subclavian artery causing limb ischaemia.
  • Other vascular occlusions – Rare causes of limb ischaemia unrelated to thoracic outlet compression.

Systemic and Red Flag Conditions

  • Pancoast tumour (apical lung tumour) – May compress the lower brachial plexus and present with arm pain and Horner’s syndrome.
  • Malignancies compressing the brachial plexus – Tumours in the neck or thorax producing similar symptoms to neurogenic TOS.
  • Cardiac conditions (e.g. angina, referred chest pain) – May present as upper chest or arm discomfort during exertion.
  • Oesophageal disorders – Can refer pain to the upper chest or neck, mimicking TOS.
  • Inflammatory or autoimmune diseases – Systemic disorders that may affect nerves or vessels and mimic TOS features.

Outcome Measures

Outcome measures are essential for assessing the severity of symptoms, functional limitations, and treatment effectiveness in individuals with thoracic outlet syndrome (TOS). These tools help guide clinical decision-making and provide objective data to monitor patient progress over time.

Diagnostic Procedures 

The diagnosis of thoracic outlet syndrome (TOS) is primarily clinical and often relies on a combination of patient history, physical examination, and provocative testing. It is important to note that TOS diagnosis is usually confirmed by the elimination of other causes with similar clinical presentation. Especially differential diagnosis of cervical radiculopathies and upper extremity entrapment neuropathies can be hard (McGillicuddy 2004).[2][12] In order to diagnose accurately, the clinical presentation must be evaluated as either neurogenic (compression of the brachial plexus) or vascular (compression of the subclavian vessels). TOS manifestations are varied, and there is no single definitive test, which makes it difficult to diagnose.[5][13]

There is no single definitive test for TOS, and false positives are common with some physical tests. A structured clinical approach is recommended, starting with a detailed history of symptom onset, aggravating factors, and functional limitations, followed by targeted examination procedures [11].

In cases of suspected neurogenic TOS, electrodiagnostic testing such as nerve conduction studies and electromyography (EMG) may be used to detect abnormalities in sensory or motor nerve function. Findings may include reduced sensory nerve action potentials or prolonged latency in the ulnar and median nerves. These tests are particularly useful in differentiating TOS from distal nerve entrapment or cervical radiculopathy [3][4].

For vascular TOS, imaging techniques are often more informative. Duplex ultrasonography, venography, and arteriography can help confirm venous or arterial compression, thrombosis, or aneurysm formation. Dynamic imaging during provocative manoeuvres (e.g. arm abduction) can improve sensitivity, particularly for effort-induced vascular TOS [14].

Plain radiographs of the cervical spine and upper thorax are typically performed to detect structural abnormalities, such as cervical ribs or elongated transverse processes. Advanced imaging, such as MRI or CT angiography, may be indicated in complex cases or prior to surgical planning [3].

A multi-modal diagnostic approach is recommended, particularly when symptoms are persistent or atypical. Diagnosis is often made by exclusion, after ruling out other conditions with similar presentations.

Examination

A thorough examination for thoracic outlet syndrome (TOS) should begin with a detailed history and be followed by physical assessment. Because of the wide variation in symptoms and the overlap with other conditions, the examination must be systematic and patient-specific [3] [11].

History

Begin by taking a comprehensive patient history to understand the onset, nature, and aggravating factors of the symptoms. This helps guide the physical assessment and can suggest which structures may be involved. Make sure to take a thorough history, clear any red flags, and ask the patient how signs and symptoms have affected his/her function.[15]

  • Onset and development over time
  • Previous trauma or overuse history
  • Type and quality of symptoms (e.g. pain, numbness, weakness)
  • Location and radiation of symptoms
  • Irritability of symptoms (ease of provocation and resolution)
  • Nature of symptoms (worse in morning, evening, or with certain activities)
  • Aggravating/alleviating factors
  • Functional impact and disability

Physical Examination

Physical examination should include both static and dynamic assessments of posture and soft tissue. The aim is to identify visible asymmetries, muscular imbalances, or vascular changes that may support a diagnosis of TOS.[7][15]

Observation and Palpation

  • Posture (head/shoulder position, scapular alignment)
  • Swelling, Oedema, or Paleness/Cyanosis (skin discolouration)
  • Muscle wasting or asymmetry
  • Temperature changes or vascular signs
  • Palpation of Supraclavicular fossa, scalene triangle, and pectoral region for tenderness

Neurological Screen

Perform a brief neurological examination to assess for nerve root involvement and differentiate TOS from radiculopathy or other entrapment syndromes.

  • Myotomal muscle strength (MMT)
  • Reflexes (if relevant)
  • Sensory testing along dermatomes
  • Neural tension testing (see Special Tests)

Muscle Assessment

Assess strength and flexibility of muscles commonly involved in TOS or contributing to compression.

Key muscles to assess:

  • Scalene muscles
  • Pectoralis major and minor
  • Levator scapulae
  • Trapezius (upper, middle, lower)
  • Sternocleidomastoid
  • Serratus anterior

Special Tests

Special tests can assist in identifying thoracic outlet syndrome (TOS), particularly when combined with a detailed history and physical examination. These tests aim to reproduce the patient’s symptoms by stressing the neurovascular structures within the thoracic outlet. They are not diagnostic on their own but may support clinical suspicion when positive[3][7].

  • Elevated Arm Stress/ Roos test - Used to provoke symptoms by maintaining a stressed position of the neurovascular bundle; commonly used for suspected neurogenic TOS.
  • Adson's - A vascular-focused test designed to assess compression of the subclavian artery, though not reliable for diagnosing neurogenic TOS.[4]
  • Wright's Test - Assesses possible compression in the costoclavicular or subcoracoid space; may provoke vascular or neurological symptoms.
  • Cyriax Release - Aimed at reproducing neurogenic symptoms by unloading the brachial plexus. May help differentiate compressive versus releasing patterns.
  • Supraclavicular Pressure Test - Applies pressure over the scalene triangle to assess for brachial plexus compression..[3]
  • Costoclavicular Manoeuvre - Evaluates for vascular and/or neurological compression between the clavicle and first rib [5]
  • Upper Limb Tension Test - Assesses neural mobility and tension along the brachial plexus and peripheral nerves.[4]
  • Cervical Rotation Lateral Flexion Test - Helps assess for the presence of a cervical rib or structural narrowing in the interscalene triangle.


These tests have variable reliability and validity. A positive result may increase clinical suspicion but should not be used in isolation. Provocative tests are most useful when combined with symptom history and other findings.

Table adapted from Gillard et al 2001[12]

Test Sensitivity Specificity LR+ LR-
Elevated Arm Stress 52-84%  30-100%  1.2-5.2  0.4-0.53 
Adson's 79% 74-100% 3.29 0.28 

Wright's

70-90% 29-53% 1.27-1.49 0.34-0.57 
Cyriax Release NT  77-97% NA NA 
Supraclavicular Pressure NT  85-98% NA NA 
Costoclavicular Maneuver NT 53-100% NA NA 
Upper Limb Tension 90% 38% 1.5  0.3 
Cervical Rotation Lateral Flexion 100% NT NA NA


Electrodiagnostic Evaluation and Imaging

Electrodiagnostic testing and imaging play an important role in the diagnosis of thoracic outlet syndrome (TOS), particularly when clinical findings are inconclusive or when differentiating between neurogenic and vascular forms is essential.

Electrodiagnostic studies, including nerve conduction velocity (NCV) and electromyography (EMG), are most useful in evaluating suspected neurogenic TOS. Findings may include reduced sensory nerve action potentials, particularly in the ulnar nerve, or denervation changes in the muscles innervated by the lower brachial plexus. However, these findings are often subtle or absent in disputed neurogenic cases [3][12].

Duplex ultrasound is increasingly recommended as a first-line imaging tool in vascular TOS, especially when symptoms are activity-related or suggestive of venous or arterial compression. This can be followed by CT angiography or MR angiography when vascular pathology is suspected or surgical planning is required [1] [12].

Plain radiographs of the cervical spine and thoracic inlet are commonly used to detect structural abnormalities, such as cervical ribs, elongated transverse processes, or first-rib anomalies [1]. Advanced cross-sectional imaging may also identify fibrous bands or muscle hypertrophy contributing to compression.

Overall, diagnostic imaging and electrodiagnostic studies are not definitive in isolation, but provide valuable supplementary information alongside clinical assessment and provocative testing.

Conclusion

TOS is a condition involving compression of the neurovascular structures as they pass through the thoracic outlet. While it remains a challenging and often controversial diagnosis, growing clinical understanding and advances in diagnostic tools have improved recognition and differentiation of its subtypes. Accurate diagnosis relies on a combination of detailed clinical assessment, appropriate imaging, and the exclusion of other potential causes. Management is often conservative, focusing on posture correction, activity modification, and physiotherapy, although surgical intervention may be indicated in selected cases. Ongoing research continues to clarify diagnostic criteria and optimise treatment strategies, contributing to improved outcomes for individuals affected by this complex syndrome.

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 Laulan J, Fouquet B, Rodaix C, Jauffret P, Roquelaure Y, Descatha A. Thoracic outlet syndrome: definition, aetiological factors, diagnosis, management and occupational impact. Journal of occupational rehabilitation. 2011 Sep 1;21(3):366-73.
  2. ↑ 2.0 2.1 2.2 2.3 Köknel TG. Thoracic outlet syndrome. Agri: Agri (Algoloji) Dernegi'nin Yayin organidir= The journal of the Turkish Society of Algology. 2005 Apr;17(2):5.
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 Hooper TL, Denton J, McGalliard MK, Brismée JM, Sizer PS. Thoracic outlet syndrome: a controversial clinical condition. Part 1: anatomy, and clinical examination/diagnosis. Journal of Manual & Manipulative Therapy. 2010 Jun 1;18(2):74-83.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J Vasc Surg. 2007;46(3):601-604.
  5. ↑ 5.0 5.1 5.2 César Fernàndez et al.; Manual Therapy for Musculoskeletal Pain Syndromes; Elsevier, 2016 
  6. ↑ Povlsen B, Hansson T, Povlsen SD. Treatment for thoracic outlet syndrome. Cochrane Database Syst Rev. 2014;(11):CD007218
  7. ↑ 7.0 7.1 7.2 7.3 Lindgren KA. Thoracic outlet syndrome. International Musculoskeletal Medicine. 2010 Mar 1;32(1):17-24.
  8. ↑ 8.0 8.1 Henry BM, Vikse J, Sanna B, Taterra D, Tomaszewski KA, Tubbs RS. Cervical rib prevalence and its association with thoracic outlet syndrome: A meta-analysis of 141 studies with surgical considerations. Clin Anat. 2018;31(1):13–23
  9. ↑ 9.0 9.1 Atasoy E. Thoracic outlet syndrome: anatomy. Hand clinics. 2004 Feb 1;20(1):7-14.
  10. ↑ 10.0 10.1 Fisher AT, Lee JT. Diagnosis and management of thoracic outlet syndrome in athletes. Semin Vasc Surg. 2024;37(1):35-43.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 Watson LA, Pizzari T, Balster S. Thoracic outlet syndrome part 1: clinical manifestations, differentiation and treatment pathways. Manual therapy. 2009 Dec 1;14(6):586-95.
  12. ↑ 12.0 12.1 12.2 12.3 Gillard J, Pérez-Cousin M, Hachulla É, Remy J, Hurtevent JF, Vinckier L, Thévenon A, Duquesnoy B. Diagnosing thoracic outlet syndrome: contribution of provocative tests, ultrasonography, electrophysiology, and helical computed tomography in 48 patients. Joint Bone Spine. 2001 Oct 1;68(5):416-24.
  13. ↑ Sandra J. Shultz et al.; Examination of Musculoskeletal Injuries; Human kinetics, 2010 
  14. ↑ Urschel Jr HC, Razzuk MA. Paget-Schroetter syndrome: what is the best management?. The Annals of thoracic surgery. 2000 Jun 1;69(6):1663-8.
  15. ↑ 15.0 15.1 Vanti C, Natalini L, Romeo A, Tosarelli D, Pillastrini P. Conservative treatment of thoracic outlet syndrome. Eura medicophys. 2007 Mar 1;43:55-70.