Bow Hunter’s Stroke
G. Michael Lemole, Jr, MD
Jeffrey S. Henn, MD
Robert F. Spetzler, MD
Joseph M. Zabramski, MD
Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona
Bow hunter’s stroke is characterized by vertebrobasilar insufficiency caused by occlusion or stenosis of the vertebral artery associated with head movements. The compromised blood flow is usually conditional upon an isolated posterior circulation with a hypoplastic, stenotic, or occluded contralateral vertebral artery and little input from the anterior circulation via the circle of Willis. The signs and symptoms of vertebrobasilar insufficiency range from dizziness, nystagmus, and nausea and vomiting to frank hemiparesis, sensory changes, Horner’s syndrome, swallowing difficulties, and loss of consciousness. Symptoms may be transient in the case of temporarily compromised blood flow or may persist when insufficient blood flow or resulting embolus or thrombus produce an infarction in the affected vascular territory. The extracranial vertebral artery usually becomes occluded when the head is rotated while the artery is fixed by surrounding bony or fibrous structures. Diagnosis usually requires dynamic studies that measure absolute or relative changes in cerebral blood flow as a result of head movement; angiography is considered the gold standard. Treatments range from conservative warnings to minimize head movement to surgical procedures designed to limit head rotation or to decompress and free the vertebral artery at the point of compression. Because the risk of a cerebrovascular accident with permanent sequela from this syndrome is significant, some form of intervention should be instituted. Patients’ medical conditions and expectations should be weighed against the severity of the disease when choosing among surgical options.
Key Words: bow hunter’s stroke, vertebrobasilar insufficiency
Bow hunter’s stroke has been defined as "hemodynamic vertebral basilar insufficiency induced by forced or voluntary rotational head movements causing intermittent vertebral artery compression at the atlanto axial level." Although the term "stroke" is used throughout the literature to refer to the condition, bow hunter’s encompasses a wide spectrum of rotational hemodynamic insuffiency ranging from a transient ischemic attack (TIA) to a frank cerebrovascular accident (CVA). As the predisposing factors, mechanisms, and pathophysiology underlying this condition have become more widely understood, more treatment options have become available. The current options of conservative treatment, surgical fusion, or vertebral artery decompression must be weighed against patients’ medical condition and personal desires. This article presents two case illustrations and reviews the natural history, diagnosis, and treatment of bow hunter’s stroke.
Figure 1. (A) Anteroposterior angiographic view of left vertebral artery with the head in neutral position. (B) With head turned to the right, the left vertebral artery occludes and contrast flow stops within the cervical vertebral artery.
A 71-year-old Caucasian female sought treatment after experiencing nausea and vertigo for 3 months. The nausea had been followed by difficulty with vision and loss of consciousness. These symptoms occurred when the patient turned her head to the right and were aggravated when she extended her head. She became dizzy when looking up into her cupboards and shelves. The patient’s medical history was remarkable only for hypertension, which had developed about 3 years earlier and was being treated pharmacologically.
On neurological examination, the patient appeared to be fully alert and oriented. Her cranial nerve function was intact, and her motor and sensory function was normal. The diagnosis of positional syncope was suspected.
Angiographic injection of the right vertebral artery revealed an occlusion from the vessel’s origin to its midcervical region. Injection of the common carotid arteries showed no evidence of blood flow through the posterior communicating arteries (PCoAs) into the posterior circulation. When the patient turned her head to the right, a transient occlusion of the left vertebral artery was observed (Fig. 1). She experienced a TIA during which she lost consciousness; she stopped breathing and her pupils dilated. When the patient’s head was returned to midline, normal blood flow through the left vertebral artery resumed and her symptoms abated. The occlusion was attributed to mechanical compromise of the artery at C1.
The patient underwent decompression of the left vertebral artery with hemilaminectomy at C1. The vertebral artery was completely freed from the sulcus arteriosus. The patient’s postoperative course was unremarkable, and she remained neurologically intact. She wore a soft cervical collar during the immediate postoperative period and has experienced no further symptoms. A follow-up angiogram obtained 3 months after surgery revealed no evidence of vertebral compromise with rotation of the head.
A 71-year-old Caucasian male sought treatment for dizziness, which occurred reproducibly, when he turned his head to the right and when he bent his head forward while playing golf. For fear of losing consciousness, he had voluntarily limited rotatory movements of his head. Previously, he had undergone bilateral carotid endarterectomies and had a history of hyperlipidemia, hypothyroidism, osteoarthritis, and an occlusion of the right central vein. His medications included clopidogrel bisulfate and aspirin.
Figure 2. (A) Anteroposterior angiographic view of the left vertebral artery with head in neutral position. (B) Turning the head to the right causes transient occlusion of the left vertebral artery.
The patient’s neurological examination was nonfocal except for a minor bilateral loss of hearing. All other cranial nerve function was intact, and motor, sensory, cerebellar, and long-tract signs were also within normal limits.
Vertebral angiographic injections demonstrated chronic occlusion of the right vertebral artery. On carotid injection, the vertebrobasilar system failed to backfill through the PCoAs. When the patient’s head was turned to the right, the left vertebral artery occluded transiently (Fig. 2A), but no symptoms manifested during the examination.