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Basilar Artery Disease
Anatomy
The two vertebral arteries merge at the pontomedullary junction to form the basilar artery (BA). This artery lies within the prepontine cistern and is the main stem of the posterior circulation. It directly supplies a large territory of vital brain tissue including the brainstem and cerebellum and provides the main conduit for blood flow to the thalami and medial temporal and parietal lobes. The BA gives rise to several groups of penetrating branches that directly supply the brainstem. The major branches are the caudally located anteroinferior cerebellar arteries (AICAs) and rostrally located superior cerebellar arteries (SCAs). The rostral portion of the BA divides into two posterior cerebral arteries (PCAs) at the pontomesencephalic junction.
There are three major groups of small penetrating arteries that leave the BA and directly supply the brainstem. The first and shortest group is the anteromedial group (i.e., paramedian perforating arteries) that penetrates the basilar sulcus. The most caudal arteries of this group at the vertebrobasilar junction are the penetrating arteries of the foramen cecum of the medulla. Rostral to these arteries are the main perforators that supply the anteromedial territory of the pons from the ventral surface to the tegmentum. The most rostral of this group are the arteries penetrating the interpeduncular fossa (i.e., inferior rami of the interpeduncular fossa) .
The second group is the anterolateral group (i.e., short circumferential perforating arteries). Arteries of this group mainly supply the anterolateral territory of the pons and do not extend to the tegmentum. The third and longest group of penetrating arteries is the lateral group (i.e., long circumferential arteries). In conjunction with small penetrators from the proximal SCA (rostrally) and proximal AICA (caudally), the long circumferential arteries supply the lateral pontine territory, extending from the ventrolateral surface to the pontine tegmentum. The most rostrolateral pontine tegmentum is supplied by the SCA alone .
The AICA is the largest circumferential branch of the BA. It usually arises from the proximal or middle segment. It first contributes penetrators (i.e., recurrent penetrating arteries of AICA) to the caudal lateral pontine territory including the exiting roots of cranial nerve (CN) VII and CN VIII and the lateral tegmentum of the pontomedullary junction. It also supplies the middle cerebral peduncle. The AICA gives off an internal auditory artery that supplies the vestibular (i.e., the vestibular artery) and cochlear (i.e., the common cochlear artery) structures of the inner ear. The AICA terminally supplies the anteroinferior cerebellum and flocculus .
The SCAs arise a few millimeters proximal to the bifurcation of the BA into the PCAs, separated by the exit of CN III, at the pontomesencephalic junction. They circle the rostral pons or caudal midbrain and divide into medial (mSCA) and lateral (lSCA) branches. The lSCA initially gives off penetrators to the rostrolateral pons and midbrain tegmentum, the superior cerebellar peduncle, dentate nuclei, and eventually the lateral portion of the superior cerebellar hemisphere. The mSCA courses around the midbrain and with the collicular artery, a branch of the PCA, supplies the colliculi and the posterior territory of the midbrain. The mSCAs further supply the superior vermis, dentate nucleus, and medial portion of the superior surface of the cerebellar hemisphere. It is important to point out that the mSCA and lSCA anastomose with the vermian and hemispheric branches of the posteroinferior cerebellar arteries (PICAs), respectively. This forms an important network of collateral blood supply that could bypass an occlusion of the BA proximal to the origin of the SCA .
Pathology and Pathophysiology
Atherosclerosis is the major contributor to BA pathologic conditions. Elevated and thickened fibrous plaques encroach upon the lumen leading to stenosis. Cracks in the plaque may lead to superimposition of red thrombi, which may occlude the artery at the point of stenosis or embolize distally. Atherosclerotic plaques may also be eccentric, representing arterial wall thickening and positive remodeling without significant compromise of the vessel lumen. These eccentric lesions can still lead to thin fibrous cap rupture, exposure of lipid core, and formation of superimposed thrombus . Negative remodeling may also occur in which arterial thickening leads to concentric narrowing or collapse of the vessel lumen .
Emboli to the BA arise from the heart, aorta (e.g., atrial fibrillation, atherosclerotic plaque of the aortic arch), or the vertebral arteries in the neck and head (atherosclerotic plaques or dissections). It may be difficult to clinically distinguish in situ thrombosis from embolism. Embolism presents suddenly without warning signs, whereas patients with in situ disease of the BA commonly present with warning signs or transient ischemic attacks (TIAs).
The New England Medical Center Posterior Circulation Registry (NEMC-PCR) prospectively studied 407 patients with posterior circulation ischemia from 1988 through 1996 . Moderate to severe BA occlusive disease was present in 109 (27%) of these patients. Three separate subgroups were identified within this population: those with isolated intrinsic BA atherostenosis (45%), those with BA disease as part of multiple artery occlusive disease found elsewhere (41%), and those with embolism to the BA without intrinsic basilar disease (14%). All groups had a high frequency of multiple vascular risk factors such as hypertension, hyperlipidemia, diabetes, smoking history, peripheral vascular disease, and coronary artery disease . The Basilar Artery International Cooperation Study (BASICS) Registry prospectively studied 519 patients with BA occlusions who received treatment in 48 centers from 2002 to 2007. Embolism was the cause of occlusion in 215 of 592 patients (36%) . This number coincides with the proportion of embolism in the NEMC-PCR when considering only complete occlusions ( n = 12/32, 38%). The NEMC-PCR also found embolism to be more common in the rostral portion, but this was limited to 12 patients .
Dissections involving the BA are relatively rare. They compose about 5–10% of vertebrobasilar intracranial dissections in several databases . The BA is more often involved as distal extensions of the intracranial V4 segment of the vertebral artery. Isolated dissections are most common in the middle or distal segment of the vessel. These dissections can extend into the AICA or SCA branches or disrupt the flow of penetrating arteries, leading to ischemia. Intracranial dissections are also prone to aneurysmal dilation and/or rupture because of the relatively poor media and adventitia compared to that of the extracranial arteries. BA dissections mostly present with ischemia rather than subarachnoid hemorrhage . Thrombosis at the site of the dissection or within the aneurysmal dilation can cause distal embolization. Often patients have multiple attacks or progressive dysfunction of the brainstem. If the aneurysmal dilation is large enough, it may also directly compress the brainstem, leading to local symptoms.
The BA may also be subject to dilatative arteriopathy, also known as dolichoectasia. The underlying abnormal connective tissue leads to the formation of vertebrobasilar nonsaccular intracranial aneurysms. Fusiform lesions are characterized as focal dilation along an isolated segment of the BA, whereas dolichoectatic BAs involve uniform dilation along the entire course of the artery. Transitional lesions are a combination of both underlying dolichoectatic changes (i.e., elongation, dilation, and tortuosity) and superimposed focal fusiform dilation . These large perturbations of BA structure lead commonly to compressive symptoms or thrombosis with ischemic symptoms. Less often they may rupture resulting in hemorrhage. Recurrence rates of ischemic stroke are high and mortality is increased except in case of strokes that are purely dolichoectatic .
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