Don’t Turn Your Head!
A 67-year-old healthy man presented for evaluation of vertigo. The patient had had intermittent vertiginous symptoms and near syncope with extreme head turning for 1 year. Previous workup included a carotid ultrasound that revealed <29% bilateral stenosis. Transcranial Doppler revealed low flow in the left vertebral artery with high velocities in the right vertebral artery; however, there was no evidence of velocity shift in the basilar artery with head turning. The patient continued to have debilitating symptoms despite conservative therapy for cervicogenic vertigo. Cerebral angiogram with head turning to the left demonstrated a normal right vertebral artery with occlusive compression at the level of the first cervical vertebral process as the artery passed through the posterior atlantooccipital membrane (Movie I of the online-only Data Supplement and the Figure). The left vertebral artery was noted to be hypoplastic with compensatory flow from the right vertebral artery. Vertebral artery stenting was not performed because of vessel tortuosity and the uncertainty of long-term outcomes in this setting. The patient was referred for spine surgery but elected to have conservative treatment.
This rare entity is classically known has bow hunter stroke or syndrome and is infrequently the cause of a common condition (syncope) faced by the cardiologist. Bow hunter stroke was originally described in 1978 by Sorenson,1 who described a patient with hemiparesis and contralateral sensory deficits during archery practice. Several mechanisms have been postulated over the past 30 years, including vertebral artery impingement from tumors, trauma, osteophyte formation, infectious processes, and fibrous bands.2,3 Fibrous bands seem to have emerged as the true cause. Previous studies have demonstrated that fibrous bands or ligaments anchor the vertebral artery typically at the C1 to C2 (atlantoaxial) level or at C6 so that cervical rotation produces occlusion of the affected vertebral artery.3 The vast majority of patients with a compromised vertebral artery never become symptomatic because of flow from the contralateral vertebral artery or the anterior cerebral circulation.
The mainstay of treatment is surgery, either posterior decompression/resection of the fibrous tissue or cervical spine fusion. Spinal fusion is universally curative; however, it comes at the cost of limited cervical spine rotation.4 Posterior decompression was performed successfully in ≈67% of patients in 1 series, with the remaining patients requiring cervical spine fusion.4 This case illustrates that selective angiography may be required for evaluation of significant neurological symptoms when noninvasive imaging is nondiagnostic. Now that angiography is available in many surgical suites, a reasonable approach would be attempted decompression followed by dynamic intraoperative angiography. If decompression proves unsuccessful, then proceeding to cervical fusion will likely eliminate the need for reoperation. For patients who elect not to have surgery, the adage “don’t turn your head” is truly one to live by.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/120/20/e162/DC1.