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Cerebellar Hemorrhage

  • Author: J Stephen Huff, MD, FACEP; Chief Editor: Helmi L Lutsep, MD  more...
 
Updated: Apr 23, 2014
 

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.

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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 occasionally 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.

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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.

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.

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Contributor Information and Disclosures
Author

J Stephen Huff, MD, FACEP Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD, FACEP is a member of the following medical societies: American Academy of Neurology, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Draga Jichici, MD, FRCP, FAHA Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada

Draga Jichici, MD, FRCP, FAHA is a member of the following medical societies: American Academy of Neurology, Royal College of Physicians and Surgeons of Canada, Canadian Medical Protective Association, Canadian Medical Protective Association, Neurocritical Care Society, Canadian Critical Care Society, Canadian Critical Care Society, Canadian Neurocritical Care Society, Canadian Neurological Sciences Federation

Disclosure: Nothing to disclose.

References
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  3. Young YR, Lee CC, Sheu BF, Chang SS. Neurogenic cardiopulmonary complications associated with spontaneous cerebellar hemorrhage. Neurocrit Care. 2007. 7(3):238-40. [Medline].

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  8. St Louis EK, Wijdicks EF, Li H. Predicting neurologic deterioration in patients with cerebellar hematomas. Neurology. 1998 Nov. 51(5):1364-9. [Medline].

  9. Mohadjer M, Eggert R, May J, Mayfrank L. CT-guided stereotactic fibrinolysis of spontaneous and hypertensive cerebellar hemorrhage: long-term results. J Neurosurg. 1990 Aug. 73(2):217-22. [Medline].

  10. Yamamoto T, Nakao Y, Mori K. Endoscopic hematoma evacuation for hypertensive cerebellar hemorrhage. Minim Invasive Neurosurg. 2006 Jun. 49(3):173-8. [Medline].

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  13. Andrews CM, Jauch EC, Hemphill JC 3rd, Smith WS, Weingart SD. Emergency neurological life support: intracerebral hemorrhage. Neurocrit Care. 2012 Sep. 17 Suppl 1:S37-46. [Medline].

 
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