The vertebral arteries, which originate as the first branch of the subclavian arteries, most commonly enter the transverse foramina at the level of C6. The arteries then course through the remaining transverse foramina and enter the intracranial compartment at the level of the foramen magnum, piercing the dura prior to their anastomosis at the vertebrobasilar junction (VBJ). Due to their passage through the transverse foramina of the cervical spine, the vertebral arteries, unlike the carotids, are tethered at multiple points along their course, resulting in varying mobility between segments. V1 (origin to C6 transverse foramen) and V3 (C2 transverse foramen to foramen magnum) represent the most mobile segments, while V2 (C6 transverse foramen to C2 transverse foramen) and V4 (foramen magnum to VBJ) are relatively fixed in place. As a result of their mobility, V1 and V3 are most commonly involved in dissections 19
. Yamaura et al. 9
further divided the V4 segment into three subdivisions: V4 (1), between C1 and dural penetration, V4 (2), between the dural penetration and the origin of the PICA and V4 (3), between the origin of PICA and the unification with the opposite VA. The authors reported involvement of VA at V4 (3) in 8/19 cases and at V4 (2,3) in 11/19 cases. None of the VADs demonstrated only V4 (1) or V4 (2) involvement in their study.
The left vertebral artery, occurring with an incidence of approximately 80%, is more commonly the dominant of the two vertebral arteries. However, multiple studies have shown the right vertebral artery to be most commonly involved in VADs 33,34
. Furthermore, the sidedness of dissection may play an important role in determining the presenting pathology. Bilateral VADs, although significantly less common, have been reported to occur in up to 15% of cases 33-35
The anatomical and histological classification of intracranial VADs has important clinical implications based on the segment of vessel dissected and the location of the mural hematoma 2
. Extracranial VADs tend to result from subintimal extravasation or extravasation between the intima and media. This most commonly results in ischemic phenomena as the pro-thrombotic sub-endothelial vessel wall is exposed to blood.
Intracranial dissection can result in both ischemic phenomena and SAH. Group 1 intracranial VADs which are limited to the V4 segment without involvement of the basilar artery are the most common. These often develop dissecting aneurysms or pseudoaneurysms resulting in SAH. Thrombotic phenomena are also possible as thrombi formed within dissecting aneurysms or pseudoaneurysms may embolize 2,5,6,23
. Less commonly VADs can extend to include the basilar artery (Group 2). These commonly result in a subintimal hematoma, thereby leading to signs and symptoms of brainstem ischemia, rather than SAH. With time, these dissections may result in an ischemic stroke or SAH several weeks or months remote from the time of the initial insult 2