Excerpt from Dissection, Vertebral Artery

Synonyms, Key Words, and Related Terms: VAD, vertebral artery dissection, stroke, aneurysm, arteria vertebralis, hematoma, carotid artery dissection, CAD

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Background: Vertebral artery dissection (VAD) is an increasingly recognized cause of stroke in patients younger than 45 years. Although its pathophysiology and treatment closely resemble that of its sister condition, carotid artery dissection (CAD), the clinical presentation, etiology, and epidemiological profile of VADs are unique.

Pathophysiology: An expanding hematoma in the vessel wall is the root lesion in VAD. This intramural hematoma can arise spontaneously or as a secondary result of minor trauma, through hemorrhage of the vasa vasorum within the media of the vessel. It also can be introduced through an intimal flap that develops at the level of the inner lumen of the vessel.

This intramural hemorrhage can evolve in a variety of ways, resulting in any of the following consequences:

The hematoma may seal off and, if sufficiently small, remain largely asymptomatic.
If the dissection is subintimal, the expanding hematoma may partially or completely occlude the vertebral artery or one of its branches. Extensive dissections (those that extend intracranially and involve the basilar artery) result in infarctions of the brain stem, cerebellum or, rarely, the spinal cord. Subintimal dissections also may rupture back into the vertebral artery, thus creating a false lumen (pseudolumen).
Subadventitial dissections tend to cause pseudoaneurysmal dilation of the vertebral artery, which may compress adjacent neurologic structures. These subadventitial dissections are prone to rupture through the adventitia, resulting in subarachnoid hemorrhage. In an autopsy series of more than 100 patients with subarachnoid hemorrhage, 5% of the hemorrhages were deemed the result of VAD.
The intimal disruption and low flow states that arise in VAD create a thrombogenic milieu in which emboli may form and propagate distally. This results in transient ischemia or infarction.

An understanding of the anatomy of the vertebral artery is helpful. The course of the vertebral artery usually is divided into 4 sections as follows:

Segment I runs from its takeoff at the first branch of the subclavian artery to the transverse foramina of cervical vertebra C5 or C6.
Segment II runs entirely within the transverse foramina of C5/C6 to C2.
Segment III, a tortuous segment, begins at the transverse foramen of C2, runs posterolaterally to loop around the posterior arch of C1, and passes subsequently between the atlas and the occiput. This segment is encased in muscles, nerves, and the atlanto-occipital membrane.
Segment IV, the intracranial segment, begins as it pierces the dura at the foramen magnum and continues until the junction of the pons and medulla, where the vertebral arteries merge to join the larger proximal basilar trunk.

Spontaneous dissection of the vertebral artery usually occurs in the tortuous distal extracranial segment (segment III) but may extend into the intracranial portion or segment IV.

Frequency:

In the US: Dissections of the extracranial cervical arteries are relatively rare. The combined incidence of both VAD and CAD is estimated to be 2.6 per 100,000. However, cervical dissections are the underlying etiology in as many as 20% of the ischemic strokes presenting in younger patients aged 30-45 years. Among all extracranial cervical artery dissections, CAD is 3-5 times more common than VAD.

Mortality/Morbidity:

VAD has been associated with a 10% mortality rate in the acute phase. Death is the result of extensive intracranial dissection, brainstem infarction, or subarachnoid hemorrhage.

Those who survive the initial crisis do remarkably well, with long-term sequelae rare.

Sex: The female-to-male ratio is 3:1.

Age: In contrast to atherothr .....