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Serious Medicine. Extraordinary Care.

Vertebral Basilar Insufficiency

Vertebrobasilar insufficiency (VBI) refers to a condition in which blood flow to the vertebral and basilar arteries is restricted, thereby providing transient insufficient blood flow to the posterior portions of the brain. The National Institute of Neurologic and Communicative Diseases defined the symptoms of VBI as: vertigo, ataxia, dizziness, syncope, drop attacks, visual disturbances and motor and sensory changes (sometimes bilateral). While VBI may be the result of a congenital abnormality, it is more commonly the result of atherosclerosis and resultant narrowing of the blood vessels. The characteristics of atherosclerotic plaque at the vertebral artery origin are unique from the morphological and pathological nature of plaque associated with the carotid. Vertebral artery plaques are often annular and concentric, hard and smooth, with minimal incidence of intramural hemorrhage or ulceration.

The Joint Study of Extracranial Arterial Occlusion as a Cause of Stroke, which examined 4,478 patients with cerebrovascular insufficiency, reported the frequency of atherosclerotic plaques was highest at the carotid bifurcation and the vertebral artery origin in a ratio of 2:1. The most common sites for atherosclerosis in the vertebrobasilar tree are at the origin of the vertebral artery and within the intradural segment. Occlusions at the vertebral artery origin tend to be asymptomatic, whereas intracranial vertebral artery lesions are more likely to be symptomatic (often in the form of a brain infarct). The mechanisms for vertebrobasilar ischemic stroke resulting from atherosclerotic lesions include hemodynamic compromise, embolism and propagation of thrombus from a recent occlusion. Approximately 20 percent of all ischemic strokes occur in the vertebrobasilar region. Embolism from distant sites is estimated to be responsible for at least half of these strokes, with vertebrobasilar atherosclerotic disease the primary etiologic factor in the remainder.

VBI may also cause a phenomenon known as subclavian steal, whereby blood is diverted from the vertebral-basilar system due to a subclavian stenosis. Subclavian steal takes place when a subclavian stenosis proximal to the origin of the vertebral artery leads to retrograde flow down the ipsilateral vertebral artery, thereby "stealing" blood from the circle of Willis, with the subsequent distal subclavian artery filling from the retrograding vertebral artery. When compensatory flow to the subclavian artery from the vertebral artery diverts too much flow toward the arm and away from intracranial structures, neurological deficits take place.

Vertebrobasilar insufficiency has been reported as the result of vertebral artery or basilar artery dissection. The dissection, either by genetic predisposition or trauma, occurs when an intimal tear in a blood vessel permits blood to enter the arterial wall and divide its layers to produce either stenosis or aneurysmal dilatation.

Diagnosis

Doppler ultrasonography is insensitive to vertebral basilar insufficiency due to the presence of surrounding bone and because the most frequent site for occlusive disease is at the vessel origin, a nonsuperficial location. The proximal vertebral artery is often tortuous, making accurate diagnosis of lesions difficult using MRA because of spin dephasing caused by turbulent flow.

Radiographic angiography is required for definitive anatomical evaluation of the involved arteries. Cerebral angiography is performed at The Nebraska Medical Center by inserting a needle into the femoral artery and then threading a wire and catheter into the vessel. A contrast agent is injected into the catheter, allowing the radiologist to clearly view the anatomy of the arteries.

Treatment Options

VBI is often treated with anti-coagulation medications. The WASID Study was a retrospective, multicenter trial comparing the efficacy of warfarin with aspirin for the prevention of major vascular events in 151 patients with a symptomatic stenosis of a major intracranial artery, followed for a median period of 14.7 months (warfarin sample group) or 19.3 months (aspirin sample group). The stroke rate for patients treated with warfarin was 3.6 per 100 patient years versus 10.4 per 100 patient years for the aspirin group, a statistically significant risk reduction. Although this study included only patients with intracranial lesions, the results are frequently extrapolated to justify systemic anticoagulation in patients with clinically symptomatic extracranial vertebral artery occlusive disease.

Three basic surgical revascularization procedures have been performed for VBI: bypass grafting (grafting a new blood vessel around the site of the narrowing), direct arterial anastomosis (transposition), and endarterectomy (plaque removal from the affected artery to increase blood flow). Because of the small size of the vertebral artery and the challenges of surgical access to this region, perioperative combined morbidity and mortality rates are high.

Endovascular access of the extracranial vertebral artery is comparatively straightforward with the added advantage of avoiding open surgery. Reviews of patients with vertebral artery disease treated by percutaneous transluminal angioplasty (PTA) suggest that proximal and mid-portion vertebral angioplasty can be carried out safely, with a reported morbidity even lower than carotid PTA. Angioplasty of the distal vertebral artery is known to have higher risks, due to the potential for occluding small perforating vessels. However, the North American Cerebral Percutaneous Transluminal Angioplasty Registry investigators report a lower angiographic success rate in dilating vertebral artery stenosis. Stenting tends to be a preferred method in treating vertebral artery stenosis. While angioplasty of basilar artery stenosis does carry the possibility of occluding the penetrating branches of the basilar artery supplying the brain stem, dramatic success has been reported in patients undergoing this endovascular treatment.