ArticleCureus2026
Imaging Spectrum of Thoracic Outlet Syndrome: A Case Series Highlighting Arterial, Venous, and Neurogenic Subtypes.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionThoracic outlet syndrome (TOS) encompasses a spectrum of neurovascular compression disorders involving the brachial plexus, subclavian artery, and subclavian vein. Diagnosis remains challenging due to variable clinical presentations and limited specificity of imaging findings, particularly in neurogenic TOS. This case series aims to demonstrate the multimodality imaging spectrum of TOS across arterial, venous, and neurogenic subtypes, compare imaging appearances among subtypes, and emphasise the importance of clinicoradiological correlation in diagnosis.
methodsThis retrospective case series was conducted at Sri Ramachandra Medical Health Centre, Chennai, Tamil Nadu, India, from January 2020 to March 2026. Eight consecutive patients with clinical suspicion of TOS (upper limb pain, swelling, venous engorgement, neurological symptoms, or ischaemic changes) underwent imaging evaluation. Imaging included Doppler ultrasound with provocative manoeuvres, computed tomography angiography (CTA), CT venography (CTV), and magnetic resonance imaging (MRI), tailored to clinical presentation. Imaging was assessed for osseous anomalies, site of compression across thoracic outlet compartments, vascular stenosis or occlusion, thrombosis, aneurysmal change, collateralisation, and indirect signs of brachial plexus compression. Results: Imaging demonstrated a broad spectrum of pathology across all TOS subtypes. Arterial TOS cases showed dynamic or fixed subclavian artery compromise, ranging from focal costoclavicular stenosis detected on CTA to long-segment chronic occlusion associated with an anomalous first rib. Venous TOS cases demonstrated subclavian vein compression at the costoclavicular space, including McCleery syndrome without thrombosis, muscular compression from a hypertrophied subclavius muscle, and chronic obstruction with extensive collateral venous channels. One patient demonstrated multi-level venous obstruction involving the subclavian and cephalic veins with associated central venous thrombosis. Neurogenic TOS demonstrated thoracic outlet narrowing due to a cervical rib with displacement of adjacent neurovascular structures on MRI. Dynamic Doppler imaging was critical in demonstrating haemodynamically significant stenosis not evident at rest. Conclusion: This case series demonstrates the broad imaging spectrum of TOS, ranging from dynamic arterial stenosis and chronic arterial occlusion to venous compression with collateralisation and indirect signs of neurogenic involvement. The cases highlight that the imaging appearance varies significantly depending on the affected structure and the site of compression within the thoracic outlet. Recognition of characteristic vascular findings such as focal costoclavicular narrowing, thrombosis, chronic occlusion, and collateral venous pathways can facilitate subtype classification and guide further management. However, imaging findings must be interpreted in conjunction with clinical symptoms, particularly in neurogenic TOS, where radiologic abnormalities may be subtle or absent.
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