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.
ubintimal 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.
