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Cerebellar Hemorrhage
Article Last Updated: Mar 13, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: J Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Editors: Draga Jichici, HBSc, MD, FRCP(C), FAHA, Assistant Professor, Department of Medicine, Division of Critical Care Medicine, McMaster University Medical School, Canada; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center; Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital; Helmi L Lutsep, MD, Associate Professor, Department of Neurology, Oregon Health and Science University; Associate Director, Oregon Stroke Center
Author and Editor Disclosure
Synonyms and related keywords:
CH, cerebellar bleeding, intracerebellar hemorrhage, stroke of the cerebellum, stroke, computed tomography, head CT, cranial CT
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. Therefore, surgical therapy was stressed.
With the availability of cranial CT, patients with milder symptoms and smaller hematomas are increasingly detected. Conservative management has been found to be effective in some of these patients. Management recommendations still are being optimized to improve outcome.
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 into tumor, blood dyscrasias, amyloid angiopathy, arteriovenous malformations, trauma, and sympathomimetic abuse are less common causes of CH.
Remote cerebellar hemorrhages are reported in patients following supratentorial surgery, spinal surgery, and in spontaneous intracranial hypotension. 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 is thought to result from transient occlusion or rupture of superior cerebellar bridging veins.
Location of the hemorrhage (midline versus 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.
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.
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
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
- 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.
Acute Stroke Management
Arteriovenous Malformations
Blood Dyscrasias and Stroke
Cardioembolic Stroke
Central Pontine Myelinolysis
Head Injury
Lacunar Syndromes
Posterior Cerebral Artery Stroke
Subarachnoid Hemorrhage
Subdural Hematoma
Syncope and Related Paroxysmal Spells
Other Problems to be Considered
Brainstem syndromes
Cerebellar infarction
Vertigo
Vestibular neuronitis
Lab 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
- CT: Acute CH should be visible as increased density in the posterior fossa (see Image 1).
- Note the location of the hematoma (central versus lobar) and any sign of brainstem compression.
- Note the absolute size of the clot in maximum diameter.
- Other signs of a posterior fossa mass include ablation of the fourth ventricle and/or compression of the ambient and quadrigeminal cisterns.
- Note any obstructive hydrocephalus.
- MRI may be important later in the clinical course to define vascular anatomy, extent of damage, and other pertinent intracranial abnormalities (eg, tumor, arteriovenous malformation).
Medical Care
- Surgical care has been the mainstay of therapy for CH, although some patients with small hematomas may be treated successfully without surgery.
- Recent efforts have focused on improving patient selection for surgery, both in identifying patients who are candidates for nonsurgical management and identifying those in whom intensive therapy is likely to be futile.
- Variation in patient selection for surgery is common, and only general guidelines are outlined here. Consultation with a neurosurgeon is indicated for all patients.
- Most investigators agree that a patient who is awake and has a Glasgow coma scale score of 14 or greater (some investigators say 9 or greater) with a small hemorrhage (some investigators say <30 mm, others <40 mm) without hydrocephalus may be a candidate for conservative supportive care with close monitoring.
- If the patient's condition deteriorates, re-evaluate and reconsider surgery.
- Clot location (medial or lateral) is also a factor in patient selection for surgery.
- Almost all agree that a patient who is comatose, flaccid, and without brainstem reflexes with a large midline hemorrhage has a poor prognosis. For such patients, supportive care without surgery may be the only indicated therapy.
- However, clear consensus does not exist regarding many patients who fall between these extremes. Variation in surgical treatment exists even within a geographic region.
- Immediate management consists of stabilization and resuscitation.
- Oxygen supplementation may be indicated.
- Perform endotracheal intubation if required for airway management in patients with a decreased level of consciousness.
- Use rapid sequence technique with precautions for increased intracranial pressure (ICP).
- Correct fluid deficit with isotonic saline.
- Mannitol 1 g/kg may be considered preoperatively in patients with tight posterior fossa.
- Persistent hypertension (mean arterial pressure >130 mm Hg) may indicate judicious use of labetalol or another titratable antihypertensive agent.
- In symptomatic bradycardia reflecting Cushing response, atropine (0.5-1 mg) may be beneficial if hypotension is present.
Surgical Care
- Indications for surgery are controversial.
- Ventriculostomy is indicated in patients with hemorrhage and hydrocephalus.
- Suboccipital craniotomy with clot evacuation is indicated in patients with altered level of consciousness and a large clot (>30 mm but no greater than 40 mm).
- Patients with a large central clot and absent brainstem reflexes have a poor prognosis. In these cases, some advocate supportive therapy only.
- Patients may appear to be in stable condition but can worsen suddenly. St Louis et al list clinical and CT findings that may identify patients who are at risk for deterioration.
- Admission systolic blood pressure greater than 200 mm Hg
- Pinpoint pupils and abnormal corneal and oculocephalic reflexes
- Hemorrhage extending into the cerebellar vermis
- Hematoma diameter greater than 30 mm
- Brainstem distortion
- Intraventricular hemorrhage
- Upward herniation
- Acute hydrocephalus
- CT-guided stereotactic fibrinolysis of the hematoma has been reported in small numbers of carefully selected patients.
- Endoscopic hematoma evacuation has also been reported to have been effective in a small number of patients.
Consultations
- Consult neurosurgery for all patients, even those who are candidates for conservative management. Sudden deterioration may require neurosurgical intervention.
- After the clinical condition stabilizes, physical therapy, speech therapy, and occupational therapy may be helpful.
No specific drug therapy exists for CH. Medications useful in treating hypertension (eg, labetalol) and increased ICP (eg, mannitol) may have a limited role in the acute phase. See the article Intracranial Hemorrhage for details.
Patients with an identified coagulopathy may require fresh frozen plasma or other products that are specific for the coagulopathy.
Further Inpatient Care
- Ideally, admit patients to the care of critical care physicians with expertise in managing intracranial hemorrhages.
- Careful monitoring for level of consciousness, vital signs, and ICP is needed for some patients.
- The risk of sudden deterioration is high and mandates the attention that is available in an intensive care unit.
- If immediate surgical intervention is deferred, a deteriorating clinical course may necessitate surgery at a later time.
- Posterior fossa craniotomy and evacuation of the hemorrhage may be necessary for patients with worsening clinical condition.
- If surgical therapy is prompt, some comatose patients still may have a good clinical outcome.
- Physical and occupational therapy may be useful in patients who are in stable condition.
Further Outpatient Care
- Physical and occupational therapy may be useful in many patients.
Transfer
- For facilities without neurosurgical care for hemorrhage management, transfer to a specialized center should occur after stabilization if the patient is viable.
- Transfer should occur only after discussion with an accepting physician.
- Transfer personnel should be skilled in critical care management.
Complications
- Progression of the hemorrhage with brainstem compression and/or destruction is the most serious complication.
Prognosis
- Prognosis is related to the size and location of the hemorrhage and the patient's clinical condition at the time of clinical presentation.
Patient Education
- For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.
Medical/Legal Pitfalls
- Failure to diagnose and delayed diagnosis following clinical deterioration are common pitfalls.
- Some patients with small, lateral CHs may experience no symptoms other than the common complaints of dizziness and headache. The natural history of this group is variable, although some undoubtedly deteriorate.
- Patients with diminished level of consciousness or intractable vomiting may be unable to cooperate with examination, making detection of cerebellar signs difficult or impossible.
- Testing the gait of any patient with a complaint of dizziness is important, particularly when dizziness is accompanied by any of the following symptoms: headache, nausea, or vomiting. CHs in the vermis may cause ataxia of the trunk without limb ataxia. Gait testing is helpful in diagnosis and is a common feature.
Special Concerns
- Patients with a coagulopathy are difficult to treat. Surgical intervention prior to correction of the coagulopathy may be disastrous, yet delaying surgery also may have risks.
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Cerebellar Hemorrhage excerpt Article Last Updated: Mar 13, 2007
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