Thoracic outlet syndrome (neurovascular compression) 2026 update

An evidence-based clinical review: Thoracic Outlet Syndrome: why the neurogenic form dominates (~95 %), how to avoid the diagnostic traps, and why 3 to 6 months of structured rehabilitation precede any surgery.

What are the fundamentals to know about thoracic outlet syndrome?🔗 Copy

The thoracic outlet syndrome (TOS, in French syndrome du défilé thoracique, SDT) is an umbrella term for a set of symptoms resulting from compression of the neurovascular structures (brachial plexus, subclavian artery and/or subclavian vein), along their course between the base of the neck and the axilla.1 Its apparent rarity hides considerable heterogeneity: one name covers diffuse neurogenic pain, acute venous thrombosis in an athlete, and arterial ischaemia that is sometimes serious. 🩺

How is this condition defined, who is affected and what are the risk factors?

Three clinical entities are distinguished according to the structure compressed, with very unequal prevalences:

• Neurogenic TOS (nTOS): ~95 % of cases. Compression of the brachial plexus, mainly in the lower trunk territory (C8-T1). Vague symptoms: cervicoscapular pain, paraesthesia in the hand (most often the ulnar border), fatigability of the upper limb during activities with the arms raised, sometimes weakness of grip.111
• Venous TOS (vTOS): 3 to 5 % of cases. Compression of the subclavian vein. Can lead to effort thrombosis or Paget-Schroetter syndrome in the young overhead athlete. Massive swelling, cyanosis, acute heaviness of the arm.8
• Arterial TOS (aTOS): < 1 % of cases, but the most serious. Compression of the subclavian artery, often associated with a cervical rib. Risk of post-stenotic aneurysm, distal embolisation, acute ischaemia.10

Epidemiological profile

TOS preferentially affects young adult women, with a female-to-male ratio of about 3:1 in adult populations, and 1,84:1 in children and adolescents (2024 paediatric meta-analysis).3 The typical age of onset is 20 to 50.4 The exact prevalence in the general population remains poorly established because there is no reference diagnostic test.

Risk factors

Anatomical / congenital 🦴 :

• Cervical rib or an elongated C7 transverse process (~0.5-1 % of the population, a major factor in aTOS).10
• Scalene muscle anomalies (hypertrophy, abnormal insertion of the anterior or middle scalene).1
• Variations in the costoclavicular or subpectoral space (anatomical narrowness).11

Acquired / functional 🏋️ :

• Trauma: whiplash , clavicle fracture (particularly a malunion), acute brachial injury.9
• Repeated microtrauma: overhead sports (swimming, baseball, volleyball, throwing), occupations with repetitive movements in elevation.12
• Prolonged forward head posture, rounded shoulders (long periods of screen work, sedentary living).1

What happens anatomically and how does TOS progress?

Compression can occur in three anatomical zones in series, from proximal to distal:

In neurogenic TOS, chronic nerve compression sustains a cycle of inflammation and fibrosis : repeated microtrauma or scalene overactivity → inflammation of the scalene muscles and surrounding tissue → formation of scar tissue (fibrosis) → perineural adhesions → restricted nerve gliding → worsening symptoms.13 This mechanism explains the insidious, chronic character of the condition.

Natural history

• nTOS: slow progression over months to years. Without intervention, chronic pain, loss of function and muscle wasting are possible in advanced cases. The majority of patients (estimated at 60 to 90 %) respond to well-conducted multimodal physiotherapy at 3-6 months; the evidence, however, remains of low to moderate quality.6
• vTOS: an immediate risk of deep vein thrombosis of the upper limb (Paget-Schroetter), with long-term complications (post-thrombotic syndrome).8
• aTOS: a risk of aneurysm and distal embolisation that can threaten the viability of the limb.10

How can thoracic outlet syndrome be assessed and diagnosed with certainty?🔗 Copy

Diagnosing TOS is notoriously difficult : no test or investigation serves as a gold standard, particularly for the neurogenic form.514 The approach rests on a rigorous history, a structured clinical examination, and reasoning by exclusion. More than 90 % of cases are neurogenic, which makes the diagnosis even more dependent on clinical assessment than on imaging.

What questions should be asked to understand the patient and their history properly?

🔍 The history is the cornerstone of the diagnosis. Four axes structure the questioning:

• Nature and topography of the symptoms: pain, paraesthesia, heaviness, weakness, change in colour. A C8-T1 distribution (4th-5th fingers, ulnar border) is common in nTOS.9
• Triggering and aggravating factors: arms raised (doing your hair, reaching shelves, painting a ceiling), prolonged driving, carrying a heavy rucksack or a shoulder bag, repetitive occupational or sporting movements in elevation.11
• Chronology: sudden vs insidious onset, remissions, total duration, any link with a traumatic event.
• History of trauma: cervical spine trauma (whiplash), clavicle fracture (particularly a malunion), 1st rib fracture, sporting or road traffic accident. Always ask about these actively.9

Which clinical tests should be carried out and which other conditions must be ruled out?

The clinical examination aims to reproduce the patient's symptoms and to exclude other conditions. Most of the provocation tests have limited reliability when used in isolation and must be interpreted as a cluster.513

📋 The most-used tests

• Roos test (EAST, Elevated Arm Stress Test): arms at 90° abduction and 90° external rotation, opening and closing the fists for 3 minutes. Reproduction of the symptoms = positive. Regarded as the most useful for nTOS, but with sensitivity/specificity varying across studies.13
• Adson's manoeuvre: loss or reduction of the radial pulse on cervical extension + ipsilateral rotation with deep inspiration. False positives are very common in asymptomatic subjects (up to 50 % in some series).5
• Wright test (hyperabduction): arm hyperabducted/externally rotated; looking for reproduction of symptoms or loss of the radial pulse. Specificity disputed.5
• Cyriax test (costoclavicular): shoulders drawn back and down (the « soldier's position »), looking for reproduction. Used within the combined clinical battery.
• Palpation of the scalenes and pectoralis minor: looking for trigger points and muscle tension reproducing the symptoms, completing the assessment.

Essential differential diagnoses

Should patients with TOS be classified, and for what benefit?

🤔 Classification into three types is essential because it entirely determines the treatment strategy and the urgency of management (the 2016 SVS consensus, still in force).2

⚠️ Critique and controversy: the challenge of diagnostic certainty

The absence of a diagnostic gold standard for nTOS is the major controversy in this condition.14 The provocation tests have poor specificity (a positive Adson in many asymptomatic people) and EMG is generally normal in « non-specific » nTOS, which is the most common form.12 The diagnosis therefore rests on a « constellation of signs and symptoms » and on a rigorous process of exclusion. The literature acknowledges both over-diagnosis (a default label applied to patients with chronic pain) and under-diagnosis (genuine cases that wander for years before the right hypothesis is raised).14

High-field (3T) MR neurography is a promising emerging tool for visualising brachial plexus compression, but its standardisation and availability remain limited (Szaro 2023 scoping review).15

Which treatment strategies are the most effective?🔗 Copy

For the neurogenic form (which accounts for > 95 % of the patients seen in physiotherapy), the international consensus is unequivocal: first-line treatment is conservative, structured over 3 to 6 months, before any invasive option is considered.26 A recent review confirms that a majority of patients report clear or complete improvement at 6 months, but the quality of the primary studies remains heterogeneous and of low to moderate level.6

Where do you start? What hierarchy of interventions?

What is the place of exercise, and is there a superior approach?

Exercise is the core of treatment. A one-size-fits-all approach is ineffective: the superior strategy is personalised and progressive, based on an assessment of the patient's individual deficits.6

Key components of an effective programme

• Stretching the tight muscles : scalenes (anterior, middle), pectoralis minor, upper trapezius, levator scapulae. Gentle, sustained stretching (30 s × 3-5 repetitions, 2-3 times/day).617
• Strengthening the scapular stabilisers : serratus anterior, lower and middle trapezius, rhomboids. Restores posture and opens the costoclavicular and subpectoral spaces.18
• Neurodynamic mobilisation (« nerve gliding ») : brachial plexus gliding techniques to restore the compliance of the nerve interfaces. Evidence of very low level (old case series).19
• Diaphragmatic breathing : reduces overactivity of the accessory scalenes, a useful accompaniment from the start and throughout the programme.20
• Cervicothoracic mobility : upper thoracic stiffness increases the load on the 1st rib and the scalenes; work on thoracic mobility into extension/rotation is often beneficial.6

Manual therapies, botulinum toxin, technologies: how effective are they?

Passive therapies are adjuncts, never treatments in isolation.

• Manual therapy: mobilisation of the 1st rib, of the upper cervical and thoracic spine, of the acromioclavicular joint; soft-tissue release (scalenes, pectoralis minor) alongside active stretching.13
• Botulinum toxin (BoNT-A) 💉: ultrasound-guided injections into the scalenes or pectoralis minor in resistant patients. The Fouasson-Chailloux 2023 systematic review (10 studies, ~555 patients) reports benefits at 1-3 months but poor methodological quality and considerable heterogeneity.7 The Woodworth 2024 SR confirms those cautious conclusions.21 To be regarded as a therapeutic window of 3-6 months for optimising rehabilitation, not as a treatment in its own right.
• Ultrasound, EMG biofeedback: possible use for postural and breathing work, but the evidence specific to TOS is very limited.
• Neuromuscular taping / kinesiotaping: a possible proprioceptive adjunct, weak level of evidence.

Summary table: modalities × level of evidence (GRADE)

Beyond the physical: how do you educate the patient and address the psychological factors?

🧠 TOS is often chronic and frustrating. Ignoring the psychosocial factors is a major cause of failure.

• A clear explanation of the condition: demystifying nerve compression, taking the drama out of it without minimising it.
• Identifying the aggravating factors and coping strategies (desk ergonomics, how a bag is carried, sporting technique, sleep).
• Adherence to the programme: improvement is gradual (weeks to months), and the home exercises are indispensable: short but regular.
• Spotting kinesiophobia, catastrophising and anxiety: predictors of chronicity to be built into management.22

⚠️ Critique and controversy

Despite the consensus on the conservative approach, the literature suffers from heterogeneous protocols (« physiotherapy » covers very variable content from one study to another).6 The 2023-2024 reviews all acknowledge low to moderate methodological quality and a lack of RCTs comparing the components (strengthening vs neurodynamics vs stretching alone).7 The effectiveness figures (« 60 to 90 % » improvement) rest on heterogeneous series with no clear control group. That uncertainty calls for transparency with the patient about timescales and the variability of individual responses.

How do you ensure lasting recovery and prevent recurrences?🔗 Copy

Resolving the initial symptoms is not enough: nTOS readily recurs when the patient returns to their previous mechanical loads without having taken on the lasting corrections. Long-term success rests on two pillars:self-management and a structured return to activity.6

How do you make the patient an active participant in their recovery through self-management?

🧠 Building independence is central. Conservative treatment achieves positive results in about 60-90 % of patients; the patient's engagement with their home programme is a key determinant. Without that ownership, the initial benefits erode quickly once supervised care ends.6

• In-depth therapeutic education: simplified anatomy, the mechanisms of compression, at-risk postures targeted at the patient's own daily life (workstation, sleep, mode of transport, how a bag is carried). Defusing fear of movement.22
• Postural awareness: learning to recognise and correct rounded shoulders and a forward head. The aim is underlying strengthening that makes « good posture » spontaneous, rather than an exhausting permanent vigilance.
• Diaphragmatic breathing done independently to manage peaks of tension and stress, at least twice a day (morning and evening, 5 minutes).20
• A personalised home programme: concise, effective, realistic (10-15 minutes maximum). A few key stretches (scalenes, pectoralis minor) + 2-3 scapular strengthening exercises + breathing. Modified progressively according to tolerance.
• Self-monitoring: identifying the early signs (paraesthesia, heaviness, early fatigue of the arm), adjusting activities without absolute rest, being extra careful during periods of stress or heavy work.
• Workstation ergonomics: screen height, armrest position, alternating sitting and standing, active breaks every 45-60 minutes.

When and how should a safe return to sport and activities be planned?

🏃 The return to demanding activities must be based on functional criteria, not on a fixed calendar. A contemporary review of the return to activity after surgical decompression confirms the importance of staged progression and of objective criteria before each step up in intensity.23

⚠️ Critique and controversy

The overall quality of the evidence on preventing recurrence and returning to sport remains weak to moderate: few RCTs, a predominance of case studies and non-randomised series. The published return-to-sport protocols (particularly in overhead athletes) remain essentially expertise-based rather than grounded in controlled clinical trials.23 The place of psychosocial factors in chronicity and recurrence is increasingly recognised but remains under-studied.22 You have to be able to admit uncertainty in front of the patient and adapt management to their context (amateur vs professional sport, physical vs sedentary occupation).

What do real clinical cases teach us?🔗 Copy

Studying clinical cases published on PubMed/PMC anchors the theoretical principles in reality. The cases below are all verifiedpublications, selected to illustrate the main variants: effort-related Paget-Schroetter, post-traumatic from a malunion, and vascular mimicry. 🧐

Case 1: Paget-Schroetter in a college lacrosse player (Kohen 2013)

📚 A college lacrosse player presents with massive swelling and cyanosis of the dominant upper limb after a run of intensive training. Doppler ultrasound confirms axillo-subclavian vein thrombosis (Paget-Schroetter syndrome). Management combines pharmacological thrombolysis and surgical decompression by resection of the 1st rib.24

Clinical lesson : venous TOS is an emergency in the young overhead athlete. Acute swelling + cyanosis after effort must raise the diagnosis immediately and trigger a vascular Doppler ultrasound. The first-contact physiotherapist (particularly in college sport) must recognise this red flag and must not offer mobilisation before vascular causes are excluded.

Case 2: Paget-Schroetter in a young swimmer (Khalid 2022)

A young adult, a recreational swimmer, presents with acute swelling of the dominant arm. Imaging reveals thrombosis of the axillo-subclavian vein on costoclavicular compression. The case, published open access in Cureus, sets out the diagnostic sequence (Doppler → MR angiography) and the treatment sequence (anticoagulation → thrombolysis → delayed surgical decompression).25

Clinical lesson : vTOS is not confined to professional athletes. Any patient doing regular overhead sport (swimming, volleyball, throwing) with unusual swelling should be considered at risk. The thrombolysis → delayed decompression sequence is the one favoured today.

Case 3: Post-traumatic TOS from clavicle malunion (Yoo 2009)

💥 A patient progressively develops neurogenic symptoms several months after a clavicle fracture that healed with a hypertrophic callus. Compression of the neurovascular bundle by the callus reduces the costoclavicular space. Management requires surgical resection of the callus in addition to rehabilitation.26

Clinical lesson : faced with a patient with progressive neurogenic symptoms and a history of clavicle fracture (even an old one, even one regarded as « healed »), palpate the clavicle and image it if necessary. A malunion is a structural cause that will respond only partly to rehabilitation alone.

Case 4: Arterial TOS presenting as Raynaud's phenomenon (Balram 2024)

🩸 A patient initially referred for presumed primary Raynaud's phenomenon (asymmetrical cooling of the fingers). Examination shows an inter-arm blood pressure asymmetry, and CT angiography reveals compression of the subclavian artery with a cervical rib and a post-stenotic aneurysm: arterial TOS. This 2024 case report illustrates how vascular presentations can be missed and mimic other conditions.27

Clinical lesson : faced with an asymmetrical« Raynaud », especially with a palpable cervical rib or a diminished radial pulse, consider aTOS and refer for a vascular workup before any symptomatic vasodilator treatment.

The diagnostic challenge: when TOS mimics another condition (Hooper 2010 review)

🤔 The clinical reviews are a reminder that a patient with C8-T1 paraesthesia can be wrongly diagnosed and treated for a C7-T1 cervical disc herniation, with treatment failure. Symptoms that are positional and overhead, a history of whiplash or clavicle fracture, and the absence of clear findings on cervical MRI should point towards assessment of the thoracic outlet.13 Conversely, TOS can also mimic carpal tunnel syndrome (distal paraesthesia) or cuff pathology (scapular pain), hence the importance of a systemic assessment rather than one focused on a single joint.

⚠️ Critique and controversy: the value and limits of clinical cases

Published cases carry a major publication bias : treatment successes are over-represented relative to failures. Over-interpretation of the provocation tests (Adson, Wright, Roos) remains common: their sensitivity/specificity in isolation is poor and using them as a cluster is more useful.5 Case reports must never replace systematic reviews in guiding standard treatment decisions.

How can these recommendations be applied in practice?🔗 Copy

Applying the recommendations runs along three axes: knowing when to refer in good time, measuring outcomes objectively, and overcoming the obstacles to implementing good practice. 🧭

When, and to which other professionals, should you refer?

One of the physiotherapist's fundamental roles, particularly in direct access, is knowing how to identify situations that fall outside their scope of practice. That decision rests mainly on screening for pathological or psychosocial « flags ».

Screening for red flags 🚩

A prospective study is a reminder that serious pathology remains rare in first-contact care.29 Verhagen's review also stresses that many classic red flags lack solid empirical validation when taken in isolation.28 The right reflex is therefore the cluster of signs, weighted by the clinical context.

Identifying yellow, blue and black flags 🟡

Psychosocial factors are major predictors of chronicity, sometimes more so than the biomechanical factors.22

• Yellow : beliefs, emotions, behaviours (catastrophising, fear-avoidance, kinesiophobia).
• Blue : work-related perceptions (low satisfaction, conflictual relationships, a sense of not being supported by management).
• Black : contextual and systemic obstacles (an insurance dispute, medico-legal litigation, rigid legislation).

The STarT Back Screening Tool, designed for low back pain, transfers as a principle of stratification: risk-stratified care is more effective and more cost-effective than standard care.30 Where psychosocial factors predominate, refer to a psychologist, an occupational physician or a social worker.

How do you measure outcomes and overcome the barriers to implementation?

Measure in order to progress 📈

• Validated PROMs : VAS / NRS for pain (0-10); DASH (30 items) or the QuickDASH (11 items) for upper limb function; SPADI for the shoulder.31
• Performance tests : grip strength (dynamometer), goniometric cervical and scapular range, quantified Roos test (maximum time without symptoms), isometric strength of the scapular stabilisers.
• Longitudinal follow-up at fixed intervals (week 1, 6, 12, 24): this supports shared patient-therapist decision-making and makes progress objective even where subjective improvement is slow.32

Overcoming the barriers to EBP 🚧

The implementation reviews identify the same barriers across countries:33

A fundamental methodological review is also a reminder that critically appraising a randomised controlled trial goes through validated scales (PEDro for physiotherapy).34 Translating knowledge into practice requires active strategies: the mere availability of guidelines is not enough.35

⚠️ Critique and controversy

🧠 While EBP is universally valued, putting it into practice raises tensions:

• The « tyranny of red flags » can lead to over-ordering of costly, anxiety-provoking imaging. The prevalence of serious pathology in first-contact care is low.29 The challenge: caution without over-medicalisation.
• Enthusiasm for PROMs can paradoxically dehumanise care if you treat the score rather than the person.
• And Interprofessional collaboration remains more theoretical than operational in siloed systems with uncoordinated payment. Breaking down those silos requires structural change beyond individual behaviour alone.