Rotational occlusion of the vertebral artery caused by transverse process hyperrotation and unilateral apophyseal joint subluxation (2024)

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“…[1][2][3] Most patients with RVAO exhibit a stenosis or anomaly (eg, hypoplasia or termination in the posterior inferior cerebellar artery) of the vertebral artery (VA) on 1 side and the dominant VA is compressed at the C1-2 level during contraversive head rotation, which compromises the blood flow in the vertebrobasilar artery territory (typical RVAO; Figure 1). [3][4][5] However, some patients may show atypical patterns, such as compression of VA at other cervical levels, [6][7][8][9][10][11] simultaneous compression of both VAs, 2,[12][13][14][15] compression of the dominant VA during ipsilateral head rotation or tilt, 6,7,10,11,16 and compression of the nondominant VA terminating in the posterior inferior cerebellar artery (PICA). [17][18][19] Based on the side of tinnitus and patterns of nystagmus induced by head rotation, transient excitation of the inner ear in the compressed VA side has been proposed as a mechanism of vertigo and nystagmus in RVAO.…”

confidence: 99%

et al. 2013

Background and Purpose-To elucidate the mechanisms and prognosis of rotational vertebral artery occlusion (RVAO). Methods-We analyzed clinical and radiological characteristics, patterns of induced nystagmus, and outcome in 21 patients (13 men, aged 29-77 years) with RVAO documented by dynamic cerebral angiography during an 8-year period at 3 University Hospitals in Korea. The follow-up periods ranged from 5 to 91 months (median, 37.5 months). Most patients (n=19; 90.5%) received conservative treatments. Results-All the patients developed vertigo accompanied by tinnitus (38%), fainting (24%), or blurred vision (19%).Only 12 (57.1%) patients showed the typical pattern of RVAO during dynamic cerebral angiography, a compression of the dominant vertebral artery at the C1-2 level during contralateral head rotation. The induced nystagmus was mostly downbeat with horizontal and torsional components beating toward the compressed vertebral artery side. None of the patients with conservative treatments developed posterior circulation stroke, and 4 of them (21.1%) showed resolution of symptoms during the follow-ups. Conclusions-RVAO has various patterns of vertebral artery compression, and favorable long-term outcome with conservative treatments. In most patients with RVAO, the symptoms may be ascribed to asymmetrical excitation of the bilateral labyrinth induced by transient ischemia or by disinhibition from inferior cerebellar hypoperfusion. Conservative management might be considered as the first-line treatment of RVAO. (Stroke. 2013;44:1817-1824.)

Bow hunter's stroke is typically due to mechanical compression or stretching of the dominant vertebral artery (VA) during contralateral head rotation against the bony elements of the atlas and axis. We report a case of vertebrobasilar insufficiency due to bilateral vertebral artery occlusion at the left C3-4 and the right C1-2 junction on rightward head rotation. A 64-year-old man experienced ischemic symptoms during 90°head rotation to the right with complete resolution of symptoms after returning his head to the neutral position. Dynamic cervical angiography with rightward head rotation showed severe compression of the right VA at the transverse foramen of C3-4 and mechanical stenosis of the left VA at the C1-2 level. During head rotation, the flow of the right VA was decreased more than the left side. Cervical 3-D computed tomography (CT) on rightward head rotation demonstrated displacement of the uncovertebral C3-4 joint, with excessive rotation of the C3 vertebral body. Based on these findings, instability at C3-4 was suspected to be the main cause of the vertebrobasilar insufficiency. Anterior discectomy and fusion at the C3/4 level were performed. Postoperatively, the patient experienced complete resolution of symptoms, and dynamic cervical angiography showed disappearance of the compression of the right VA. To our knowledge, this is the first reported case of bow hunter's stroke diagnosed by dynamic cerebral angiography and cervical 3-D CT without angiography, and treated by anterior decompression and fusion without decompression of the VA.

The authors present a case of traumatic, complete, high cervical spine injury in a patient with gradual worsening deformity and neck pain while in rigid cervical collar immobilization, ultimately resulting in coronal-plane spondyloptosis. Due to the extent of lateral displacement of the spinal elements, preoperative evaluation included catheter angiography, which revealed complete right vertebral artery (VA) occlusion. A prophylactic arterial bypass graft from the right occipital artery to the extradural right VA was fashioned to augment posterior circulation blood supply prior to reduction and circumferential instrumented fusion. Following surgery, the patient was able to participate in an aggressive rehabilitation program allowing early mobilization, and he ceased to be ventilator-dependent following implantation of a diaphragmatic pacer. The authors review factors leading to progression of this type of injury and suggest technical pearls as well as highlight specific management pitfalls, including operative risks.