Although many imaging techniques are used to document<unk> s, their pathogenesis remains controversial. It may involve various mechanisms such as systemic hypotension, microemboli, severe arterial stenosis, ICA occlusion or a combination of these. Anatomy Outer surface of cerebral hemisphere, showing areas supplied by cerebral arteries. Pink is the region supplied by the middle cerebral artery, blue is supplied by the anterior cerebral artery and yellow is supplied by the posterior cerebral artery. Cortical<unk> s occur at the borders between those areas. These events are localized to two primary regions of the brain: # Cortical<unk> s (CWS), or outer brain infarcts, are located between the cortical territories of the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). # Internal<unk> s (IWS), or subcortical brain infarcts, are located in the white matter along and slightly above the lateral ventricle, between the deep and the superficial arterial systems of the MCA, or between the superficial systems of the MCA and ACA. Nonetheless, within the literature itself, there exists confusion over the terminology used to describe cortical (outer brain) infarcts and subcortical (inner brain) infarcts. Besides<unk> , border-zone is another common term used to refer to areas of the brain between the ends of two adjacent arteries. Other less used terms include: borderland, end zone, boundary zone, and terminal zone. These varying terms have arisen from the considerable anatomic variability both in the cerebral vascular structure and the territories of the brain that they supply. Hypotension A sharp drop in blood pressure is the most frequent cause of<unk>  infarcts. The most frequent location for a<unk>  is the region between the anterior cerebral artery and middle cerebral artery. These events caused by hypotension do not usually cause the blood vessel to rupture. Microemboli Microemboli have not been experimentally proven to cause<unk> s. It is unclear whether they are a cause or an effect of a<unk> . With<unk> s, platelet aggregates block the small meningeal arteries in<unk>  regions creating a microembolism. Microemboli usually form as thrombi, and can block arteries outright. On the other hand, they often detach, move into blood circulation, and eventually block smaller downstream branches of arteries causing a thromboembolism. Generally, emboli travel as far outward as their size permits along the vascular branches of the brain. Using this hypothesis, microemboli are viewed as the cause of the infarct rather than secondary events. Nevertheless, secondary thrombi do form after infarcts, and therefore it has been difficult to distinguish between emboli and thrombi in<unk>  locations. The best supporting evidence is correlative; patients display subcortical abnormalities on CT scans and present more microembolic signals during a carotid endarterectomy. Microemboli can be common in some high-risk patients, such as those with carotid stenosis. However, in healthier patients strokes do not usually result from microemboli. ICA occlusions Thrombi at the split of the internal carotid artery in the neck may cause<unk>  infarcts between the territories of the anterior cerebral artery and the middle cerebral artery. The resulting<unk>  infarcts in carotid artery blockages have mostly been considered to be due to a reduced blood flow, similar to that of hypotension. Imaging studies in severe internal carotid artery (ICA) disease report an incidence of<unk>  ranging from 19% to 64%. Almost 40% of these<unk>  infarcts are attributed to narrowing of the carotid artery, which produces the reduced blood flow. However, a different possible explanation has emerged. Alternatively, the vascular occlusion could be the result of microemboli from the carotid thrombi before the lumen becomes completely blocked. In this scenario, the clotting becomes too severe and the clot breaks free. The resulting traveling clot is known as an embolus (plural emboli). The wall of internal carotid artery just distal to the bifurcation (split) is a common site of atherosclerosis because of the unique hemodynamic effects caused by the blood flow divider. As a result, thrombi formation is more prevalent there. In general, researches have observed that this microembolization is a frequent phenomenon during the build-up of cerebral thrombi. The resulting emboli are pieces of calcified plaque. If these microemboli are 0.1 mm in diameter, they might pass into the small branches of the vascular system. There they may be destroyed by protective cellular defenses, or they may cause a stroke. Altogether, these considerations suggest that the<unk>  infarcts in carotid thrombosis are caused by microembolization from mural thrombi, thrombi adherent to the vessel wall, rather than by blood flow disturbances.
Watershed stroke
Lacunar stroke
ROSAH syndrome
Posterior cerebral artery syndrome
Middle cerebral artery syndrome
Anterior cerebral artery syndrome
Posterior circulation infarct
Perisylvian syndrome