Cerebellar Hemorrhage

Background
Advances in neuroimaging have led to revision of treatment concepts for cerebellar hemorrhage
(CH). In the precomputed 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 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.

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.

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
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.[3]

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.

Differential Diagnoses

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

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

CT: Acute CH should be visible as increased density in the posterior fossa.

Large hemorrhage of cerebellar vermis.

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. There has been a call for large
prospective randomized controlled trials to determine best treatment.[4]
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 diameter, others < 40 mm diameter) without hydrocephalus may be a
candidate for conservative supportive care with close monitoring. (See the Glasgow Coma
Scale calculator.)
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 remain controversial.[5]

Ventriculostomy may be indicated in patients with hemorrhage and hydrocephalus but is
controversial as well.[5]
Suboccipital craniotomy with clot evacuation is indicated in patients with altered level of
consciousness and a large clot (see discussion in Medical Care; clot size >30-40 mm in
greatest diameter).
American Heart Association/American Stroke Association guidelines previously gave a
high-level recommendation for surgical removal of hematoma smaller than 30 mm in patients
who are deteriorating neurologically or have brain stem compression and/or hydrocephalus from
ventricular obstruction,[6, 7] but a specific size recommendation is lacking in more recent
recommendations.[5, 7]
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.[8]
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
Clot evacuation and direct fibrinolysis of the hematoma has been reported in small
numbers of carefully selected patients.[9, 10, 11, 12]
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.

Medication Summary

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. There is great heterogeneity in clinical practice for treatment of
patients with intracerebral hemorrhage regarding blood pressure management, treatment of
coagulopathy, and treatment of patients on antiplatelet therapy. Though no specific information
addresses consideration of patients with cerebellar hemorrhage, it seems reasonable to
extrapolate some concepts. For patients on antiplatelet therapy, transfusion of platelets or
treatment with desomopressin (DDVAP) may be considered.[13] Further study is needed.

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 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.

http://emedicine.medscape.com/article/1163554-overview
Contributor Information and Disclosures
Author
J Stephen Huff, MD Professor of Emergency Medicine and Neurology, Department of
Emergency Medicine, University of Virginia School of Medicine
J Stephen Huff, MD is a member of the following medical societies: American Academy of
Neurology,American College of Emergency Physicians, and Society for Academic Emergency
Medicine
Disclosure: BrainScope Grant/research funds Other; Banyan Grant/research funds Other

Specialty Editor Board

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, Canadian Congress of Neurological Sciences, Canadian Critical Care
Society, Canadian Critical Care Society, Canadian Medical Protective Association, Canadian
Medical Protective Association, Canadian Neurocritical Care Society, Neurocritical Care
Society, Royal College of Physicians and Surgeons of Canada, and Society of Critical Care
Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska
Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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 Academy of Neurology, American Heart Association, American Medical
Association, American Neurological Association, American Society of
Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical
Association

Disclosure: Nothing to disclose.

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments
of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of
Medicine
Selim R Benbadis, MD is a member of the following medical societies: American Academy of
Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology
Society,American Epilepsy Society, and American Medical Association
Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking,
consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking,
consulting; Sleepmed/DigiTrace Honoraria Consulting; Sunovion Consulting fee None;
Supernus Speaking, consulting; Upsher-Smith Grant/research funds None

Chief Editor
Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and
Science University School of Medicine; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of
Neurologyand American Stroke Association
Disclosure: Stryker Neurovascular Consulting fee Review panel membership