Although many imaging techniques are used to document watershed strokes, their
pathogenesis remains controversial. It may involve various mechanisms such as systemic hypotension,
microemboli, severe arterial stenosis, ICA occlusion or a combination of these. With watershed strokes,
platelet aggregates block the small
meningeal arteries in watershed 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 watershed 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.
Internal carotid artery occlusion Thrombi at the split of the internal carotid artery in the neck may cause watershed infarcts between the territories of the anterior cerebral artery and the middle cerebral artery. The resulting watershed 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 watershed stroke ranging from 19% to 64%. Almost 40% of these watershed 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 watershed infarcts in carotid thrombosis are caused by microembolization from mural thrombi, thrombi adherent to the vessel wall, rather than by blood flow disturbances. ==Diagnosis==