Because of its unique position abutting the brainstem, infarction of the cerebellum can lead to a compression of the fourth ventricle with resulting hydrocephalus, direct compressive brainstem injury, and downward brainstem herniation, all with devastating neurologic consequences ( Fig. 43.1 ). Vulnerable patients are those with large cerebellar infarctions associated with mass effect, typically caused by occlusion of the posterior inferior cerebellar artery or by occlusion of multiple cerebellar branch arteries. In the latter case, involvement of the vermis is associated with an increased risk of neurologic deterioration. Treatment is surgical decompression with suboccipital craniectomy, and placement of an external ventricular drain if there is hydrocephalus. Intervention must be performed urgently when signs of brainstem dysfunction are present to prevent progressive injury.
In patients at risk, close observation for signs of neurologic deterioration is mandatory. Serial brain computed tomography (CT) may be useful for monitoring the degree of mass effect and hydrocephalus. If neurologic signs or symptoms referable to brainstem dysfunction appear and are associated with a correlating change in the degree of compression on imaging, surgery should be pursued urgently. At times there may be uncertainty as to whether clinical signs of brainstem dysfunction are in fact due to brainstem compression, for instance when a significant change on serial imaging is not apparent. In these cases, osmotic therapy such as a bolus of mannitol can be given; if there is improvement in symptoms, this argues strongly to proceed with decompressive surgery.
In some patients, progressive swelling becomes apparent on serial scans without an obvious clinical change. Prophylactic decompressive surgery should be considered in these cases, as waiting until clinical symptoms appear carries some risk of irreversible brain injury.