eMedicine Specialties > Neurology > Neurological Emergencies
Cerebellar Hemorrhage
Updated: Dec 11, 2008
Introduction
Background
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.
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, and sympathomimetic abuse are less common causes of CH.
Cerebellar hemorrhages are rarely reported in patients following supratentorial surgery, spinal surgery, and in patients with spontaneous intracranial hypotension.1,2 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.
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.
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.
Clinical
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)
- Irregular respirations
- Extensor plantar responses
- Impaired oculocephalic responses and a variety of other abnormal eye movements
- Decreased or absent corneal responses
- Impaired or absent pupillary responses
- Lateralizing cerebellar signs may be present in a patient who is alert enough to cooperate with examination.
- Limb ataxia
- Dysarthria
- Possible presence of extensor plantar responses (unilateral or bilateral)
- Nuchal rigidity
- Nystagmus
- Gaze palsy (ipsilateral to hematoma)
- Facial weakness
- Noncardiac or neurogenic cardiopulmonary complications may include findings of pulmonary edema, hypertension, bradycardia, and arrhythymia.3
- Diminished level of consciousness (uncooperative to comatose)
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
- 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.
More on Cerebellar Hemorrhage |
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| Differential Diagnoses & Workup: Cerebellar Hemorrhage |
| Treatment & Medication: Cerebellar Hemorrhage |
| Follow-up: Cerebellar Hemorrhage |
| Multimedia: Cerebellar Hemorrhage |
| References |
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Further Reading
Keywords
CH, cerebellar bleeding, intracerebellar hemorrhage, stroke of the cerebellum, stroke, computed tomography, head CT, cranial CT
