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Subaxial Vertebral Artery Entrapment by Thyroid Cartilage and C5: Why Radiologists Should Think Beyond Bow Hunter’s Syndrome—A Case Report
By Farnaz Delavari, Patrik Michel, Vincent Dunet and 1 others.
Abstract
Background and Clinical Significance: Bow Hunter’s syndrome is an uncommon cause of vertebrobasilar insufficiency caused by dynamic vertebral artery narrowing during head rotation or extension. It is classically described at the atlantoaxial level, whereas subaxial compression is less recognised. Thyroid cartilage-related vertebral artery compression is particularly rare and may mimic vertebral artery dissection on static imaging. This case highlights the need to distinguish anatomical conflict from clinically causal haemodynamic compression. Case Presentation: A 51-year-old man with vascular risk factors and a well-anticoagulated mechanical aortic valve presented with three transient ischaemic attacks within two hours, including left-hand paraesthesia, right hemianopia, transient aphasia, and right-hand paraesthesia. Symptoms occurred spontaneously, without clear relation to head or neck movement or trauma. Doppler ultrasound showed normal carotid and vertebral flow. CT angiography demonstrated focal stenosis of the right vertebral artery at the V1–V2 junction caused by an osteocartilaginous “pincer” between the right thyroid cartilage ala and the C5 transverse process. The axial appearance mimicked vertebral artery dissection, but multiplanar CTA and contrast-enhanced MRA supported external indentation without mural haematoma, intimal flap, pseudoaneurysm, or double lumen. Perfusion CT showed no focal hypoperfusion, and diffusion-weighted MRI showed no acute infarct. Because symptoms were not positional and competing embolic risk factors were present, conservative management was chosen. Conclusions: Thyroid cartilage-related subaxial vertebral artery compression is a rare diagnostic pitfall. Static imaging may suggest dissection or Bow Hunter’s syndrome, but causality should not be inferred without compatible symptoms, exclusion of alternative mechanisms, and, when needed, dynamic confirmation.



