![]() Presenting neurologic deficits are primarily determined by the physiologic function of involved vascular territories (see figure and table). Finally, subdural hematomas, which usually stem from tears in bridging veins between the dura and arachnoid mater, can lead to focal neurologic deficits. Secondary hemorrhagic conversion can also occur from ischemic infarcts, as well as from damaged tissue due to tumor or trauma. These usually occur spontaneously, especially in patients with long-standing hypertension or those taking anticoagulants or antiplatelet agents. In contrast to ischemic strokes, hemorrhagic strokes are usually caused by arterial bleeding that directly damages brain tissue or obstructs vascular flow through elevated local pressure. Cerebral venous thrombosis can cause obstructed venous outflow resulting in infarction or hemorrhage. Emboli can also disseminate from the venous circulation in the presence of a right-to-left shunt such as a patent foramen ovale. Emboli that originate from the heart occur due to pump failure, or due to irregular heart rhythm that disrupts smooth blood transit through the heart as in atrial fibrillation or atrial flutter. These can be due to atherosclerosis or other vasculopathies, including arterial dissections, typically of the vertebral arteries in cerebellar strokes. The thrombotic phenomenon can occur in large or small vessels, and thromboembolic can travel from large to small vessels. These can be further subdivided by the source of the obstruction in the blood vessel, either through migration from the heart or directly at the vasculature. Ischemic strokes are caused by arterial obstructions that impair blood and oxygen delivery directly. ![]() Like all strokes, cerebellar infarcts are roughly divided into ischemic and hemorrhagic events.
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