Cerebellar Hemorrhage

Updated: Apr 19, 2022
  • Author: Sonal Mehta, MD; Chief Editor: Helmi L Lutsep, MD  more...
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Practice Essentials

Cerebellar hemorrhages (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 CH. Approximately two thirds of CHs are believed to be hypertensive hemorrhages.

Signs and symptoms

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


Acute CH should be visible on CT scan as a hyperdensity in the posterior fossa.

MRI may be important later in the clinical course to define vascular anatomy, extent of damage, and other pertinent intracranial abnormalities


Surgical care has been the mainstay of therapy for CH, although some patients with small hematomas may be treated successfully without surgery. 

No specific drug therapy exists for CH. Medications useful in treating hypertension (eg, labetalol, nicardipine, clevidipine) and increased ICP (eg, mannitol) may have a limited role in the acute phase.



Advances in neuroimaging have led to revision of treatment concepts for cerebellar 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.



Cerebellar hemorrhages (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.




An estimated 10% of intracerebral hemorrhages are believed to be cerebellar in location. An estimated 1–2% of strokes are CHs.

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 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]


In US population studies, CH is more common in blacks than in other races.

No gender predilection exists for CH.

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.



Infratentorial hemorrhages affecting the brainstem and cerebellum have been associated with poor prognosis. [5]  A study further analyzing these hemorrhages by location found that brainstem hemorrhages are associated with higher mortality and morbidity in comparison to cerebellar hemorrhages (CHs). [6]

Prognosis is largely related to the size and location of the hemorrhage and the patient's clinical condition at the time of clinical presentation.


Patient Education

For patient education resources, see the Stroke Center, as well as Stroke.