Particular attention paid to thoracic, abdominal, and systemic complaints and findings can lessen concern for other immediate life-threatening conditions such as trauma, aortic dissection, acute coronary syndrome, pulmonary embolism, hypovolemia, or sepsis. Presenting symptoms of a cerebellar infarction are often nonspecific and overlap with other neurologic, cardiovascular, gastrointestinal, and systemic conditions. Since intracranial pressure builds from the choroid plexus superiorly where cerebrospinal fluid is synthesized and transmitted downwards through the remainder of the brain, obstructing the fourth ventricle can thus also create tremendous downward pressure and lead to disastrous herniation of the cerebellar tonsils into the foramen magnum. Alternatively, edema can also obstruct the fourth ventricle and aqueducts anteriorly, causing direct brainstem compression. Swelling can lead to upward transtentorial herniation of the cerebellar vermis to relieve the rising intracranial pressure. The cerebellum sits in the relatively tight cranial space of the posterior cranial fossa, between the tentorium cerebelli above it and the occipital bone behind and beside it, with the foramen magnum below and the fourth ventricle and brainstem in front. Reactive cerebral edema surrounding the territory of an initial infarct can be especially problematic as it evolves in the case of cerebellar strokes. However, presentations can often be atypical or overlap, in particular for hemorrhagic infarcts. Finally, obstruction of the superior cerebellar artery (SCA, located most rostral) tends to produce more ataxia, dysarthria, and nystagmus, with less vertigo, headache, and vomiting. Anterior inferior cerebellar artery (AICA) territory infarction more often leads to dysmetria, Horner's syndrome, unilateral hearing loss and ipsilateral facial paralysis or anesthesia with contralateral hemibody sensory loss of pain and temperature. From caudal to rostral, obstruction of the posterior inferior cerebellar artery (PICA, also the most frequent location for a cerebellar infarct) leads to a headache and less commonly vomiting, vertigo, horizontal ipsilateral nystagmus, and truncal ataxia. 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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