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Ischemic brain infarctions involving the anterior circulation are by far the most common type of ischemic stroke due to the relative amount of blood that flows to this area as opposed to the posterior circulation. Mechanisms causing anterior circulation cerebral infarction can be separated into three broad categories: cardiogenic embolism, artery-to-artery embolism, and hemodynamic insufficiency due to low perfusion.
Cardiogenic embolism accounts for about 25% of all ischemic strokes and is usually due to atrial fibrillation (either paroxysmal or sustained). Other mechanisms postulated in formation of cardiogenic emboli include left atrial appendage thrombus, paradoxical embolism via a patent foramen ovale, and aortic arch plaque embolism. Emboli tend to involve large- and medium-sized anterior circulation arteries and collect at bifurcations and trifurcations (e.g., middle cerebral artery (MCA) bifurcation/trifurcation, top of the basilar, posterior cerebral artery (PCA)). Emboli may also spontaneously thrombolyze themselves due to natural intrinsic thrombolytics processes resulting in emboli to smaller penetrating arteries.
In up to 25% of cases of suspected brain embolism, a cause cannot be found giving way to a new term in stroke neurology, Embolic Stroke of Undetermined Source (ESUS). Currently clinical trials are underway to determine optimal treatment for patients with ESUS.
Artery-to-artery embolism can also occur. The source is usually the carotid artery bifurcation where atherosclerotic disease tends to occur resulting in plaque formation and subsequent emboli. Intracranial stenosis that usually occurs in the MCA can result in thrombosis and embolism as well giving rise to different stroke syndromes.
The aortic arch divides into three branches: the left common carotid artery, the left subclavian artery, and the brachiocephalic trunk which gives rise to the right subclavian and right common carotid artery.
“The internal carotid arteries arise from the common carotid artery at the carotid bifurcation. The internal carotid artery (ICA) and its main branches supply the cerebral hemisphere and part of the deep, subcortical areas. The origin of the ICA in the neck at approximately C4–C5 makes it readily accessible to examination by auscultation (for bruit) and noninvasive vascular studies. Atherosclerosis is the predominant condition affecting the extracranial ICA and is restricted to the first 2 cm of its origin. Fibromuscular dysplasia and dissection of the carotid arteries are other causes of artery-to-artery embolism emanating from the carotid artery.
Obstructive lesions at the site may cause hemodynamic changes in the distal regions of the hemispheric blood supply, in the so-called border zones between the major cerebral circulations [anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA)], or may serve as a source of intraarterial embolism obstructing the intracranial circulation” (from previous edition).
The ICA passes through the petrous temporal bone and the cavernous sinus and reaches the subarachnoid space at the base the brain. It divides into the middle and anterior cerebral arteries but before this bifurcation it gives rise to the anterior choroidal artery and the PCA.
The anterior choroidal artery is long and thin and supplies the optic tract, parts of the choroid plexus and cerebral peduncle, and deeper areas such as parts of the internal capsule and hippocampus. The posterior communicating artery joins the PCA (which is part of the vetebrobasilar system).
The ACA supplies the medial aspect of frontal and parietal lobes.
The large MCA supplies the lateral aspect of the cerebral hemispheres including the precentral gyrus, postcentral gyrus, and insula. It is divided into an M1 and M2 branch followed by deeper branches.
Large arteries such as the MCAs can be prone to emboli being lodged at the M1 or proximal MCA or at the bifurcation between the M1 and M2 arteries. Atherosclerosis can also occur in the proximal MCA. Large emboli to the M1 branch are being removed using embolectomy given recent data showing the efficacy of this type of procedure.
There are small perforating arteries supplying the deep cerebral structures. These smaller arteries are subject to atherosclerosis in the form of lipohyalinosis that causes smaller deep infarcts. These so-called “lacunar” infarcts can result in pure motor or pure sensory syndromes if the anterior circulation perforators are involved.
Even with the development of sophisticated neuroimaging techniques, lesion localization in stroke neurology has remained central to the diagnosis and management of stroke syndromes. In the acute phase, localization is essential to the accurate diagnosis of cerebral dysfunction in a vascular territory as well as to rarer manifestations of stroke allowing the planning of acute interventions.
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