Vertebral Artery Disease

Epidemiology and Pathophysiology

The most common vascular disease affecting the proximal portion of the VA is atherosclerotic plaque formation. Often stenosis begins in the SA and spreads into the orifice of the V1 segment, although in situ plaque formation is also common ( Fig. 83.2 ). Proximal ECVA disease is often multiple and accompanied by occlusive disease of the carotid artery as well as the brachiocephalic, coronary, or peripheral limb vessels. Even when V1 stenosis is severe, it rarely leads to hemodynamically mediated brain infarction because of the high potential for collateral formation with the surrounding muscular branches of the ECVA, in addition to the thyrocervical trunk and external carotid artery branches. Embolism from ECVA stenosis is an important cause of brainstem and cerebellar infarction and is the mechanism through which ECVA-origin disease causes strokes. Hemodynamically mediated transient ischemic attacks (TIAs) are common but brief and usually abate with time . Bilateral proximal stenosis or occlusion carries a higher risk of stroke but is almost never seen in isolation and, in general, severe deficits or death are attributable to severe intracranial occlusive disease that accounts for the strokes . Several risk factors have been identified as contributors to ECVA atherosclerotic disease, such as concomitant peripheral, aortic, and coronary artery diseases; hypertension; hypercholesterolemia; smoking; and being a white male.

Other conditions that can lead to stroke originating in this portion of the VA include arterial dissections and aneurysms that have been shown to harbor clots with the potential to embolize distally. The distal ECVA segments (V2 and V3) rarely contain significant atherosclerotic lesions. Disease in these segments most often involves mechanical and physical perturbation of the vessel, such as arterial dissections, trauma, mechanical compression, and stretching related to head position . Dissection is a common entity that affects the mobile segments of the vessels causing a tear and subsequent bleeding within the media of the arterial wall. The intramural hematoma can dissect longitudinally and can potentially tear through the intima exposing the hematoma to the arterial lumen. This situation can lead to activation of the coagulation cascade with subsequent distal embolization in the posterior circulation. The intramural hematoma also has the potential to expand, occluding the lumen and leading to hypoperfusion and brain infarction. Most often, the ECVA segment affected is the distal atlas loop portion of the vessel before it pierces the dura. A number of activities have been associated with the increased risk of dissection, which include but are not limited to trauma, forced prolonged neck postures such as those sustained in surgeries or resuscitation, and neck manipulation by chiropractors. However, at times, seemingly benign movements can function as triggers. Finally, VA injury within the intervertebral foramina has been well characterized in situations such as traumatic accidents causing facet joint dislocations. Proximal retrograde propagation of the clot from the site of the vessel injury has been documented in these cases. Atlantoaxial dislocation with secondary vessel compression due to motor vehicle accidents or conditions such as rheumatoid arthritis and Klippel–Feil syndrome as well as suicidal hangings and cervical osteophyte formation have been reported as more rare causes of V3 compression.