hemorrhage (CH). In the pre–computed tomography (CT) era, patients with large
hematomas (which were detected by angiography or at postmortem examination) were
overrepresented in clinical series. Surgical therapy was stressed. With the availability of
cranial CT, patients with milder symptoms and smaller hematomas are increasingly
detected. Nonsurgical management has been found to be effective in some of these
patients. Management recommendations are still being optimized to improve outcomes.
Pathophysiology
CHs result from the same causes as other intracerebral hemorrhages. Long-standing
hypertension with degenerative changes in the vessel walls and subsequent rupture is
believed to be the most common cause of a typical cerebellar hemorrhage.
Hemorrhage from tumors, blood dyscrasias, amyloid angiopathy, arteriovenous
malformations, trauma, sympathomimetic abuse, and genetic disorders such as
CADASIL are less common causes of CH. [1]
Cerebellar hemorrhages are occasionally reported in patients following supratentorial
surgery, spinal surgery, and in patients with spontaneous intracranial hypotension. [2, 3] The
mechanism is thought to be removal of large amounts of cerebrospinal fluid (CSF) or
continuing CSF leak from dural breach. The hemorrhage is remote from the surgical site or
anatomic defect and may result from transient occlusion or rupture of superior cerebellar
bridging veins.
Location of the hemorrhage (midline vs hemispheric) is important in determining symptoms
and clinical course. It may be more important than absolute hematoma size for prognosis.
Generally speaking, the more lateral the hemorrhage and the smaller the hematoma, the
more likely the brainstem structures are spared and the better the prognosis.
Development of obstructive hydrocephalus from ventricular compression may lead to
increased intracranial pressure and decreased cerebral perfusion pressure.
Brainstem damage by compression from an expanding mass in the posterior fossa is a
common and feared complication.
Epidemiology
Frequency
United States
An estimated 10% of intracerebral hemorrhages are believed to be cerebellar in location.
An estimated 1-2% of strokes are CHs.
International
Up to 30-45% of strokes are intracerebral hemorrhages in some Chinese and Japanese
series. Approximately 10% of these may be cerebellar in origin.
Mortality/Morbidity
Mortality rates are unknown but are related to the size of the hematoma, location, and
compression of adjacent brainstem structures. In one study, researchers found mortality
was closely linked to the level of consciousness. Only 1 out of 8 non-comatose patients
died, whereas 10 out of 18 comatose patients died. [4]
Race
In US population studies, CH is more common in blacks than in other races.
Sex
No gender predilection exists for CH.
Age
CH may occur at any age, depending on the etiology. Generally, incidence increases with
age; most hypertensive hemorrhages occur in patients older than 50 years. Rupture of a
vascular malformation may be the most common cause in children.
History
Onset of symptoms is generally abrupt.
Presentation varies greatly, depending on the size and location of the hemorrhage. Some
patients are alert with headache and perhaps vomiting; others may be unresponsive with
impaired or absent brainstem reflexes.
The following symptoms are roughly in descending order of incidence:
Headache of abrupt onset
Nausea and vomiting
Inability to walk (reflecting truncal ataxia)
Dizziness, vertigo
Dysarthria
Nuchal pain
Loss or alteration of consciousness
Physical
Physical examination findings also are variable. Some patients are alert and cooperative,
while others are in a coma.
Signs generally are of abrupt onset and may change suddenly with progressive expansion
of hematoma.
Signs tend to cluster with level of consciousness.
Diminished level of consciousness (uncooperative to comatose)
o Irregular respirations
o Extensor plantar responses
o Impaired oculocephalic responses and a variety of other abnormal eye
movements
o Decreased or absent corneal responses
o Impaired or absent pupillary responses
Lateralizing cerebellar signs may be present in a patient who is alert enough to
cooperate with examination.
o Limb ataxia
o Dysarthria
o Possible presence of extensor plantar responses (unilateral or bilateral)
o Nuchal rigidity
o Nystagmus
o Gaze palsy (ipsilateral to hematoma)
o Facial weakness
Gait difficulty in patients able to cooperate is a nonspecific finding.
Noncardiac or neurogenic cardiopulmonary complications may include findings of
pulmonary edema, hypertension, bradycardia, and arrhythmia. [5]
Causes
Causes are similar to those of other types of intracranial hemorrhage. Approximately two
thirds of CHs are believed to be hypertensive hemorrhages.
Hypertension - Suspected rupture of small penetrating vessels
Amyloid angiopathy
Anticoagulant use
Blood dyscrasias
Aneurysm/arteriovenous malformation rupture
Sympathomimetic drug use
Hemorrhage into tumor
Dural leak or large CSF removal associated with supratentorial surgery, spinal
surgery, or spontaneous intracranial hypotension.
CADASIL [1]
Differential Diagnoses
Acute Management of Stroke
Acute Subdural Hematoma in the ED
Blood Dyscrasias and Stroke
Cardioembolic Stroke
Central Pontine Myelinolysis
Emergent Management of Subarachnoid Hemorrhage
Head Injury
Lacunar Syndrome
Posterior Cerebral Artery Stroke
Laboratory Studies
Obtain coagulation studies and a platelet count in all patients, particularly those taking
anticoagulant medication.
Obtain other admission laboratory work (including a specimen for blood type and
crossmatch) if surgery is a possibility.
Imaging Studies
Computed tomography
Acute CH should be visible as a hyperdensity in the posterior fossa.