2026 年 13 巻 p. 457-462
Bow Hunter's syndrome results from rotational insufficiency of the vertebral artery. Though traditionally associated with C1-C2 level compression, subaxial cervical causes are increasingly recognized. We report a 68-year-old man with codominant vertebral arteries presenting with dizziness and transient visual disturbances during head rotation. Imaging showed severe focal stenosis caused by an osteophyte at the left C3-C4 facet joint. Dynamic angiography revealed that the left vertebral artery was nearly occluded during rotation; despite faint distal residual flow, contrast failed to reach the basilar artery. The patient underwent a left C3-C4 facetectomy and posterior C2-C5 fusion. Intraoperative angiography confirmed restoration of antegrade flow, and the patient's symptoms resolved postoperatively. Identifying the underlying hemodynamic mechanism and selecting an appropriate surgical route are important for the successful management of this condition.
Bow Hunter's syndrome (BHS) is a rare entity caused by rotational occlusion of the vertebral artery (VA). Dynamic compression or stenosis of the VA induced by head rotation can result in vertebrobasilar ischemia, potentially leading to brainstem or cerebellar infarction with permanent neurologic deficits. Classically, BHS has been recognized as a disease primarily caused by osteoarthritic changes in the atlantoaxial spine. In their systematic review, Rastogi et al.1) reported that approximately 70% (69.7%; 99 of 142 cases) occurred at the atlantoaxial (C1-C2) level, identifying the transitional area from the V2 segment to the V3 segment as the most common site of VA occlusion.
However, advances in imaging modalities, including three-dimensional computed tomography (3D-CT) for detailed visualization of the spatial relationship between osseous structures and the vertebral artery (VA), and dynamic angiography, have improved the understanding of its pathophysiology. Recent systematic reviews have shown that subaxial cervical involvement (C3-C7) now accounts for more than half of all reported cases, surpassing the C1-C2 level involvement overall.2,3) Within the subaxial cervical spine, VA compression is predominantly attributed to osteophytes in the uncinate process (53%). In contrast, mechanical compression due to facet joint hypertrophy is distinctly rare, occurring in only 13.8% of subaxial cervical cases.3)
Although identifying the exact ischemic mechanism via dynamic evaluation is crucial for these positional symptoms, the optimal surgical strategy for the lesions located dorsal to the VA remains a subject of debate. The C3-C4 segment represents a biomechanical transitional point where the 3D kinematics shift from the lower mobility C2-C3 joint to the high-mobility subaxial segments.4,5) Ishii et al.4) demonstrated that axial rotation nearly doubles from the C2-C3 level (2.2°± 0.9°) to the C3-C4 segment (4.5°± 1.1°). This abrupt increase in rotational range, coupled with peak lateral bending (5.4°± 1.3°) and extension (2.3°± 1.7°) at this level, amplifies the dynamic mechanical stress concentrated at this specific junction.4)
Despite this, BHS originating specifically from facet joint hypertrophy at this level remains poorly characterized in the literature. Here, we report a rare case of BHS caused by superior articular process (SAP) hypertrophy at the C3-C4 level. Although the patient had well-developed bilateral VAs, the left VA became nearly occluded during head rotation, resulting in symptomatic vertebrobasilar insufficiency. We further discuss the possible mechanisms underlying ischemic events in this setting and provide a technical rationale for posterior decompression and stabilization as a definitive treatment for this high-mobility junction.
A 68-year-old White male with a history of hypertension, hyperlipidemia, obstructive sleep apnea, pulmonary embolism (>5 years before presentation), and recent stroke (7 months before initial evaluation) presented to an outside hospital with episodic dizziness, lightheadedness, imbalance, and transient visual disturbances. Symptoms were positional and exacerbated by neck extension. Initial computed tomography angiography (CTA) of the head and neck demonstrated near-occlusion of the left VA (Figure 1A and B). He was subsequently referred to our institution for further evaluation.
Preoperative three-dimensional computed tomography angiography (3D-CTA).
A: Initial axial CTA from the referring facility, demonstrating severe facet joint hypertrophy at the C3-C4 level (orange arrow).
B: Initial coronal CTA image from the referring facility, demonstrating apparent occlusion of the left VA (yellow arrow) caused by an osteophyte originating from the C3-C4 hypertrophied facet joint.
C: Repeat axial CTA at our institution demonstrating severe focal narrowing of the left VA secondary to severe facet joint hypertrophy at the C3-C4 level (orange arrow).
D: Repeat coronal CTA at our institution, demonstrating severe focal stenosis of the left VA (yellow arrow) caused by an osteophyte originating from the hypertrophic C3-C4 facet joint.
VA: vertebral artery
On presentation, he reported recurrent episodic vertigo, dizziness, and presyncope triggered by leftward head rotation, neck extension, suboccipital pressure, and overhead arm positioning. Repeat CTA at our institution demonstrated severe focal stenosis of the left VA at the C3-C4 level, secondary to facet joint hypertrophy (Figure 1C and D). Dynamic cerebral angiography was therefore performed to further evaluate hemodynamics.
Dynamic angiography revealed severe stenosis of the left VA at the V2 segment in the neutral position. With leftward head rotation and extension, there was position-dependent near-complete occlusion at the C3-C4 level, with transient reconstitution at the V2-V3 junction, and distal flow attenuation. During provocative maneuvers, antegrade opacification of the basilar artery was lost, indicating functional vertebrobasilar flow compromise. Retrograde flow from contralateral VA to the left V4 segment was also observed (Figure 2A-D).
Preoperative dynamic digital subtraction angiography (DSA).
A: Anterior-posterior view of the right VA in the neutral position, showing normal baseline flow.
B: Anterior-posterior view of the left VA in the neutral position, showing severe focal stenosis in the V2 segment (yellow arrow).
C: Right VA during leftward rotation. Antegrade flow is maintained, with retrograde flow into the distal left VA observed via the vertebrobasilar junction (white arrow).
D: Left VA during leftward rotation. Though contrast opacification is visible distal to the C3-C4 level (yellow arrow), it fails to reach the basilar artery (red arrow).
VA: vertebral artery
Posterior decompression with left C3-C4 total facetectomy (Figure 3A) and C2-C5 instrumentation was planned because the V2 segment at the C3-C4 level was dorsally compressed by facet hypertrophy (Figure 3B). The surgery was performed in a hybrid operating suite with real-time intraoperative angiographic monitoring. Intraoperative angiography prior to incision confirmed preserved antegrade flow in the left VA at the left C3-C4 level.
Pre- and postoperative imaging, surgical planning, and intraoperative assessment of C3-C4 facetectomy and VA flow restorations.
A: 3D-CT reconstruction (lateral view) illustrating the surgical planning for bone resection.
The red area indicates the planned resection of the C3 inferior articular process (IAP), and the yellow area represents the planned resection of the C4 superior articular process including the osteophyte (superior articular process [SAP]).
B: Preoperative sagittal CT demonstrating the SAP of C4 (yellow arrow) compressing the left VA from behind at the C3-C4 level.
C: Postoperative sagittal CT demonstrating complete resection of the facet complex and successful decompression of the left VA (yellow arrow).
D: Intraoperative digital subtraction angiography (DSA) prior to the decompression, illustrating significant narrowing in the left VA at the C3-C4 level (yellow arrow).
E: Intraoperative DSA after the decompression, demonstrating immediate recovery of robust antegrade blood flow in the left VA (yellow arrow).
3D-CT: three-dimensional computed tomography; CT: computed tomography; VA: vertebral artery
C2-C5 instrumentation was first performed under CT-based navigation guidance, followed by a complete left C3-C4 facetectomy using high-speed drilling and micro-dissection techniques (Supplementary Video 1, Figure 3C).
After removal of the inferior articular process of C3, navigation guidance was used to confirm depth and proximity to the transverse foramen. The SAP of C4 and the associated osteophyte complex were then resected to achieve complete decompression of the VA.
Doppler ultrasonography confirmed the patency of the left VA following decompression. Intraoperative angiography subsequently demonstrated immediate improvement in luminal caliber and antegrade flow of the left VA at the C3-C4 level (Figure 3D and E). No intraoperative complications occurred.
The patient was discharged on post-operative day 2 in a stable condition and reported complete resolution of position-dependent symptoms at follow-up.
In this case, despite similar diameters of the bilateral VAs and balanced contributions to the basilar artery, neurological symptoms occurred exclusively during head rotation, when the left VA became nearly occluded. Zaidi et al.6) reported that 36.4% of patients with symptomatic BHS exhibited excellent flow from the contralateral VA. They discussed that symptoms in these patients may be transient in the case of temporary reduction in blood flow or may be continued when the insufficient blood flow or a resulting embolus causes ischemia in the affected area.6) The exact pathophysiology remains unclear; however, two potential mechanisms may be considered: (1) artery-to-artery embolism and (2) impaired vertebrobasilar autoregulation.
First, repetitive dynamic compression of the already stenotic left VA by the hypertrophic C3-C4 facet joint may have caused endothelial injury, potentially leading to thrombus formation and artery-to-artery embolism. Although this mechanism is plausible in the setting of mechanical vascular irritation, repeated diffusion-weighted imaging studies make it difficult to confirm definitively. Nevertheless, the potential involvement of transient microembolism cannot be entirely ruled out, as it could contribute to the development of position-dependent symptoms without leaving detectable ischemic changes on imaging.
Second, impaired vertebrobasilar autoregulation may have contributed to symptom development. Okada et al.7) reported that patients with vertebrobasilar insufficiency due to V1 segment stenosis maintain high stump pressure, averaging approximately 87% of systemic arterial pressure, reflecting robust collateral capacity. However, they further suggested that even this excellent autoregulatory capacity may be insufficient and can be overwhelmed in the setting of abrupt VA occlusion during postural changes.
Although the site of compression in this case was the V2 segment, the underlying hemodynamic principle is likely similar. As Zaidi et al.6) mentioned, a mismatch between blood flow and cerebral oxygen demand resulting from the compromise of the affected VA can trigger a wide range of neurological symptoms. We hypothesize that head rotation-induced dynamic occlusion, superimposed on preexisting stenosis, reduced pressure beyond the autoregulatory capacity, thereby triggering vertebrobasilar insufficiency.
Selection of surgical approach to BHS according to the spinal levelsAlthough BHS has traditionally been attributed to pathology at the atlantoaxial spine,1,8) subaxial cervical involvement (C3-C7) is now recognized in over half of the reported cases, highlighting the need for level-specific surgical strategies.3,5,6)
At the C1-C2 level, the pathology is primarily driven by the wide rotational range of the atlantoaxial joint, whereas subaxial cervical BHS is more commonly caused by focal mechanical compression by bony structures such as osteophytes, facet joint hypertrophy, or soft tissues like fibrous bands or cartilage. When conservative measures, such as bracing or activity modification, fail to provide symptomatic relief, surgical intervention should be tailored to the underlying mechanism.
Endovascular treatment has a limited role in this condition. Although vessel sacrifice by coil embolization may be effective in embolic disease, it is not suitable for flow-related dynamic compression.9) Moreover, stenting in highly mobile cervical segments carries a risk of structural failure, potentially resulting in acute thrombosis, thromboembolism, or vessel occlusion due to repetitive mechanical stress. For example, in Eagle's syndrome, external mechanical compression by an elongated styloid process has been reported to cause stent-related complications, including fracture of stents deployed in the internal carotid artery.10-12) In this case, the marked hypertrophy of the C3-C4 facet joint suggests that a purely endovascular approach may carry a potential risk of mechanical compromise in this highly mobile segment, thereby favoring surgical decompression and instrumentation.
Surgical strategy should be determined by the anatomical location of compression. Posterior approaches are typically used for V3 segment lesions at C1-C2, where the VA is most vulnerable as it exits the C2 transverse foramen and loops over the atlas under conditions of extreme atlantoaxial rotation. Conversely, anterior approaches are more frequently applied to V2 segment pathology, as approximately 53% of subaxial cervical cases are associated with uncinate process osteophytes, located anterior to the VA. Thus, the surgical approach should be determined by the anatomical location and mechanism of the compression. Although Schunemann et al.13) suggested that an anterior cervical discectomy and fusion may be a safer option with a lower risk of iatrogenic VA injury, their reported case did not involve a direct bony compressive lesion such as an osteophyte or disc herniation, and symptoms were attributed to dynamic stretching of the VA, which improved with stabilization alone without decompression. Liu et al.14) reported complication rate of 7% for anterior approach and 4% for posterior approach in the treatment of cervical radiculopathy, although the difference was not statistically significant. However, anterior approaches carry specific risks, including dysphagia, and recurrent laryngeal nerve palsy, which are particularly relevant in older patients due to the risk of aspiration and reduced postoperative quality of life.14)
With an anterior approach, the VA and the cervical nerve root are located directly anterior to the offending osteophytes, and surgical decompression may increase the risk of iatrogenic injury to these structures. In contrast, the posterior approach allows direct access to the offending osteophytes as part of facetectomy, without manipulation of the VA or nerve root.
One limitation of the posterior approach involving a facetectomy is the need for longer cervical fusion. In this case, C2-C5 fusion was unavoidable because complete C3-C4 facetectomy precluded effective screw placement in the left C3 and C4 lateral masses.
Although this construct required multilevel fusion, the posterior approach provided a favorable safety profile for this severe dynamic pathology. In addition, the use of intraoperative navigation and vascular imaging enabled precise anatomical orientation and helped minimize the risk of iatrogenic injury.
ConclusionWe report a case of subaxial cervical Bow Hunter's syndrome (BHS) caused by C3-C4 facet joint hypertrophy. This case highlights that symptomatic vertebrobasilar insufficiency may occur even in the presence of codominant VAs when dynamic occlusion exceeds the limits of vertebrobasilar autoregulation. Careful hemodynamic assessment is therefore highly recommended in patients with position-dependent symptoms. In case of dorsally located compressive lesions, a level-specific posterior approach can be considered an effective and viable treatment option.
The authors declare no conflicts of interest.
Informed consent was obtained from all patients included in the study.
