Management of Cerebellar Hematomas and Infarcts

Cerebellar Hemorrhage

Cerebellar hemorrhage is most often seen in known hypertensive patients, and the most common site of bleeding is in the area of the dentate nucleus, presumably from rupture of a branch of the superior cerebellar artery . The hematoma thus begins in the cerebellar hemisphere, although it may extend medially to involve the vermis or the contralateral hemisphere, and therefore may dissect into the fourth ventricle, resulting in intraventricular hemorrhage . Direct involvement of the brain stem is unusual, but brain stem compression from mass effect, as is seen in both cerebellar hemorrhage and infarction, is not only common, but is the major cause of morbidity and mortality from these conditions.

Besides hypertensive hemorrhage, other etiologies of a cerebellar hematoma need to be ruled out. Patients with hereditary, acquired, or iatrogenic coagulopathies are at significantly increased risk for cerebellar hemorrhage. Underlying structural causes of hemorrhage may be present in any patient, but are most common in younger patients, in nonhypertensive patients, or in patients with hematoma localized to the cerebellar vermis ( Fig. 153.1 ). Structural causes of hemorrhage would include primary or metastatic brain tumors, vascular anomalies, sterile or septic thromboemboli and, related to the above, hemorrhagic transformation of a cerebellar infarction. A careful search for an underlying structural cause needs to be made in all patients who present atypically, according to the criteria mentioned. In our experience, a traumatic etiology for cerebellar hemorrhage (as opposed to supratentorial traumatic hemorrhage) is extremely rare and has been seen only in association with major head trauma ( Fig. 153.2 ). The exception to this rule would be patients with coagulopathies who may have either spontaneous cerebellar hemorrhage or cerebellar hemorrhage associated with very minor head trauma.

The signs and symptoms of cerebellar hemorrhage are very similar to those for cerebellar infarction and, once again, relate to the resultant mass effect in the posterior fossa. Heros has outlined the following three major stages that form the hallmarks of the clinical presentation of posterior fossa mass effect . In the early stage, symptoms are related to destruction of cerebellar tissue and/or extension of hematoma into the subarachnoid space. These symptoms include dizziness, nausea, vomiting, headache, balance difficulties, and gait ataxia. These symptoms are more likely to be of an abrupt onset in cerebellar hemorrhage, and are more likely to be of a stuttering nature or insidiously progressive in cerebellar infarction. Patients in the early stage of the posterior fossa compression process are still relatively awake and alert.

The intermediate stage of posterior fossa compression ensues when mass effect increases and/or hydrocephalus results from either direct compression of the fourth ventricle or from extension of blood into the ventricular system with blockage of the cerebrospinal fluid pathways. This stage is marked by a depression of the level of consciousness and other neurological findings referable to increased intracranial pressure, including abducens nerve palsies. A mild hemiparesis and peripheral facial nerve deficit, from compression of the facial colliculus, as well as Babinski’s sign, may be detectable at this time.

In the late stage of posterior fossa compression, coma ensues. At this point, brain stem compression is maximal and cardiovascular abnormalities are seen. Patients may progress rapidly through the three stages of posterior fossa compression particularly when significant hydrocephalus or large masses are present. This compounds the precarious nature of their medical management and has led to a great interest in optimizing treatment for both cerebellar hemorrhage and cerebellar infarction with early surgical intervention in appropriate cases.