Rotational vertebrobasilar insufficiency secondary to vertebral artery occlusion from fibrous band of the longus coli muscle

Abstract

Rotation-induced vertebrobasilar artery hypoperfusion causes transient ischemic attacks (TIAs), affecting the cerebellum, brainstem and spinal cord. When these symptoms occur transiently due to head movement, compression of the vertebral artery by an extraluminal lesion should be suspected. Cervical spondylotic spurs and anterior scalene muscle or deep cervical fascia are among the factors which can compress the vertebral artery. When symptoms of vertebrobasilar insufficiency occur with rotational head movement, subclavian angiography for visualization of the entire vertebral artery in both neutral and rotated head positions should be undertaken.

Rotational Vertebral Artery Occlusion

“…6,34 Three-dimensional CT angiography throughout head rotation may help to identify the surrounding structures and fibrous bands compressing the VA. 17,32 At the subaxial level, the VA from the origin to its entrance into the foramen transversarium at C6 can be compressed by the anterior scalene and longus colli muscles, deep cervical fascia, and cervical sympathetic chain. 2,[6][7][8][9] When the VA passes through the foramina transversaria of the cervical vertebrae at C6-C2, it is susceptible to compression by osteophytes and other degenerative changes of cervical spondylosis.…”

“…[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.…”

Comparison of left and right vertebral artery intracranial diameters

“…This has been reported in the literature to occur in some cases of manipulation of the cervical spine involving repeated, extreme extension andlor rotation movements of the head and neck (Beatty, 1977;Bladin and Merory, 1975;Bolton et al, 1989;Braun et al, 1983;Dadsetan and Skerhut, 1990;Danek, 1992;Easton and Sherman, 1977;Fast et al, 1987;Frisoni and Anzola, 1991;Frumkin and Baloh, 1990;Krueger and Okazaki, 1980;Lyness and Wagman, 1974;Okawara and Nibbelink, 1974;Parkin et al, 1978;Schellhas et al, 1980;Shimizu et al, 1988;Terrett, 1987;Thiel, 1991;Yang et al, 1992).…”

Angiographic Assessment of Rotational Vertebral Artery Syndrome (Bow Hunter's Syndrome): A Case Series

“…Symptoms commonly include transient dysarthria, dysmetria, al-tered consciousness, drop attacks, nausea, ataxia, vision changes, headache, nystagmus, and tinnitus. [1][2][3][4][5][6][7][8][9][10][11][12][13] RVAS has been reported to result in dissection and thrombus formation. Emboli from the vertebrobasilar system have caused infra-and supratentorial infarctions in locations such as the cerebellum, primary visual cortex, thalami, and temporal lobes.…”