About 20% of cerebellar infarcts are space occupying. The expanding po
sterior fossa mass causes direct brain stem compression, hydrocephalus
by occlusion of the fourth ventricle, and sometimes upward transtento
rial herniation. This results in secondary brain stem symptoms and an
increasing disturbance of consciousness two to four days after the str
oke. Coma, posturing, ataxic respiration may develop within 24 hours.
So patients must be monitored in an intensive care unit. It seems evid
ent now, that many patients with massive cerebellar infarction only su
rvive by neurosurgical intervention. Decompressive suboccipital cranie
ctomy with removal of infarcted tissue is the most propagated surgical
procedure. Nevertheless, there is no general agreement about the opti
mal timing and type of surgical intervention at present.