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Journal Article
Endovascular Embolization of a Nondominant Vertebral Artery Compressed by an Osteophyte to Prevent Recurrence of Vertebrobasilar Infarctions.
Journal of Stroke and Cerebrovascular Diseases : the Official Journal of National Stroke Association 2015 September
BACKGROUND: Vertebral artery compression by cervical osteophyte is a rare cause of vertebrobasilar ischemic stroke. This mechanism of stroke has been reported as the Bow Hunter syndrome defined by vertebrobasilar insufficiency because of mechanical stenosis of the vertebral artery at the cervical level triggered by head movement. The most common treatment is surgical decompression. However, in most cases, a dominant vertebral artery is involved, and its dynamic extrinsic compression is demonstrated on angiography.
CASE REPORT: We report a patient with recurrent posterior circulation infarctions because of the compression of a nondominant vertebral artery by a cervical osteophyte. The dynamic angiography did not show any worsening of the vertebral stenosis by head movements but an irregularity of the vertebral artery with regard to the osteophyte compression, suggesting a direct artery wall injury. We concluded to an embolic mechanism through thrombus formation from the artery wall injury at the stenosed site. Because neither surgical decompression nor stenting was deemed to be a relevant treatment option, endovascular coil embolization of the compressed vertebral artery was performed after a clamping test to check the efficiency of the collateral circulation. The procedure was a success. During the 12-month follow-up, the patient did not have any recurrent stroke.
CONCLUSIONS: In case of recurrent symptomatic extrinsic compression of a nondominant vertebral artery, endovascular embolization after a clamping test may be considered.
CASE REPORT: We report a patient with recurrent posterior circulation infarctions because of the compression of a nondominant vertebral artery by a cervical osteophyte. The dynamic angiography did not show any worsening of the vertebral stenosis by head movements but an irregularity of the vertebral artery with regard to the osteophyte compression, suggesting a direct artery wall injury. We concluded to an embolic mechanism through thrombus formation from the artery wall injury at the stenosed site. Because neither surgical decompression nor stenting was deemed to be a relevant treatment option, endovascular coil embolization of the compressed vertebral artery was performed after a clamping test to check the efficiency of the collateral circulation. The procedure was a success. During the 12-month follow-up, the patient did not have any recurrent stroke.
CONCLUSIONS: In case of recurrent symptomatic extrinsic compression of a nondominant vertebral artery, endovascular embolization after a clamping test may be considered.
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