Journal of neuroendovascular therapy · 2026
Ischemic Stroke Caused by Vertebral Artery Compression at C1 with a Floating Thrombus in an Incomplete Arcuate Foramen.
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Miyata Kei, Fujita Shogo, Yamaguchi Yoshitaka, Takada Tatsuro, Shimbo Daisuke, Oki Sogo, Asaoka Katsuyuki
Аннотация
OBJECTIVE: Vertebral artery (VA) compression associated with an arcuate foramen (AF) is a rare cause of ischemic stroke. We report a case of ischemic stroke caused by VA compression at the C1 level with a floating thrombus, highlighting the pathophysiology and treatment strategy.
CASE PRESENTATION: An older woman presented with vertigo and gait disturbance. MRI demonstrated acute infarcts in the bilateral posterior inferior cerebellar artery (PICA) territories. Angiographic studies revealed focal stenosis with a floating thrombus in the left VA at the C1 level (V3 segment), associated with compression by adjacent bony structures, as well as a stenotic lesion in the right VA at the V2 segment. CTA demonstrated external compression of the left VA associated with a left incomplete AF. Serial MRA demonstrated fluctuating visualization of the right vertebrobasilar system before treatment. Given that posterior circulation perfusion depended on the dominant right VA and hemodynamic compromise was suspected, revascularization of the right VA with stent placement was performed first to improve antegrade flow. This was followed by elimination of the embolic source by parent artery occlusion of the left VA in the same session.
CONCLUSION: VA compression associated with an AF may result in ischemic stroke primarily through artery-to-artery embolism, with possible contribution from hemodynamic compromise. Treatment strategies should be tailored based on both the embolic mechanism and the hemodynamic status of the vertebrobasilar circulation.
CASE PRESENTATION: An older woman presented with vertigo and gait disturbance. MRI demonstrated acute infarcts in the bilateral posterior inferior cerebellar artery (PICA) territories. Angiographic studies revealed focal stenosis with a floating thrombus in the left VA at the C1 level (V3 segment), associated with compression by adjacent bony structures, as well as a stenotic lesion in the right VA at the V2 segment. CTA demonstrated external compression of the left VA associated with a left incomplete AF. Serial MRA demonstrated fluctuating visualization of the right vertebrobasilar system before treatment. Given that posterior circulation perfusion depended on the dominant right VA and hemodynamic compromise was suspected, revascularization of the right VA with stent placement was performed first to improve antegrade flow. This was followed by elimination of the embolic source by parent artery occlusion of the left VA in the same session.
CONCLUSION: VA compression associated with an AF may result in ischemic stroke primarily through artery-to-artery embolism, with possible contribution from hemodynamic compromise. Treatment strategies should be tailored based on both the embolic mechanism and the hemodynamic status of the vertebrobasilar circulation.