Purpose Bow Hunter’s syndrome (BHS), also known as rotational occlusion of the vertebral artery, contributes to posterior circulation ischemia secondary to dynamic compression of the dominant vertebral artery. This entity is most commonly attributed to cervical spondylosis or atlantoaxial hypermobility. The purpose of this case report is to illustrate an iatrogenic cause of BHS following cervical spine surgery. In addition, we emphasize the importance of using provocative DSA in diagnosing this condition in the setting of posterior circulation ischemia.

Materials and methods 74 year old male presented in 2011 with a complaint of right upper extremity weakness and imaging findings of C1–2 instability and myelomalacia of the cervical spinal cord. The patient subsequently underwent C1–6 posterior fusion by orthopedic surgery and recovered uneventfully with initial postoperative radiographs demonstrating intact hardware. Routine 9 month follow-up radiographs revealed a fractured left C1 pedicle screw. 11 months post-op, patient developed transient visual symptoms prompting MRI of the brain, which was normal.

The patient had a fall in early 2012 and the next cervical spine radiographs demonstrated fractures of both C1 screws, 14 months post-fusion. Over the next year, the patient presented to the ED multiple times for falls and eventually developed slurred speech and an unsteady gait. MRI brain revealed multiple posterior circulation infarcts of varying ages. CTA and MRA of the neck revealed a focal area of 30% stenosis of the left V3 segment. Conventional angiography without provocative maneuvers demonstrated a chronically occluded right vertebral artery and 30% stenosis of the distal left vertebral artery, interpreted as atherosclerotic. Despite maximal medical therapy including aspirin and plavix, in January 2015 he again developed new symptoms with decreased responsiveness, blurred vision, and right sided weakness. CTA of the neck demonstrated extrinsic compression of the left V3 segment due to adjacent fractured screw fragment. MRI revealed progression of the posterior circulation ischemic changes with no lesions in the carotid territories. Given the concern for extrinsic compression by the adjacent screw fragment, repeat DSA was requested.

Results Right subclavian arteriogram with blood pressure cuff inflated again demonstrated chronic occlusion of the right vertebral artery. Left vertebral artery injection performed with the patient’s head in neutral position revealed 50% stenosis of the left vertebral artery V3 segment adjacent to the fractured screw, as seen on CTA. A provocative maneuver was then performed by having the patient turn his head to the left. Angiogram showed complete occlusion of the left vertebral artery confirming the diagnosis of BHS. Final angiogram with his head in neutral position showed flow had been restored.

Conclusion We have demonstrated an elusive case of iatrogenic BHS. CTA and MRA are the primary imaging modalities for vascular assessment in the setting of cerebral ischemia. However, DSA with provocative maneuvers is an essential tool and may have led to an earlier diagnosis in this patient if performed on the initial angiogram. There should be an increased index of suspicion for BHS in patients with history of cervical spine surgery and infarcts confined to the posterior circulation.

Disclosures P. Gulotta: None. G. Bennett: None. J. Milburn: 3; C; Penumbra.