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
Diagnosis
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
Management
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/Morbidity
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]
Demographics
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.
Onset of cerebellar hemorrhage (CH) 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:
Causes of cerebellar hemorrhage (CH) are similar to those of other types of intracranial hemorrhage. Approximately two thirds of cerebellar CHs are believed to be hypertensive hemorrhages.
Hypertension - Suspected rupture of small penetrating vessels
Amyloid angiopathy[8]
Anticoagulant use
Blood dyscrasias
Aneurysm/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.[9]
Acute cerebellar hemorrhage (CH) should be visible as a hyperdensity in the posterior fossa.
View Image
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, and the volume of the hematoma.
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.
Follow-up imaging is generally recommended routinely within a 24-hr period, or immediately in case of any neurologic change, to evaluate for hematoma expansion, mass effect, or developing hydrocephalus.
Vascular imaging such as CT angiography, MR angiography, or catheter angiography of the intracranial vessels should be obtained to rule out the presence of an arteriovenous malformation, fistula, or aneurysm
CT angiography in acute CHs may demonstrate a "spot sign." In one study, amongst patients treated conservatively, the spot sign was seen in 12% of cases and was associated with larger hematomas, faster hematoma expansion, and worse functional outcome. The same study found that amongst patients treated surgically, the spot sign was more frequently seen, in 23% of patients, and was associated with higher mortality. CT angiography might thus serve as a useful prognostic tool as well.[10]
Magnetic resonance imaging
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, CAA[8] ).
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.
Hyperosmolar therapy with mannitol or hypertonic saline may be considered preoperatively in patients with a tight posterior fossa, although not much data exist to support these agents.
Persistent hypertension (mean arterial pressure > 140 mm Hg) may indicate judicious use of labetalol or another titratable antihypertensive agent, such as nicardipine or clevidipine.[11]
In symptomatic bradycardia reflecting Cushing response, atropine (0.5–1 mg) may be beneficial if hypotension is present.
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.[12]
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. In addition to neurologic deterioration, development of brainstem compression or hydrocephalus are indications for surgical treatment.[13]
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. For infratentorial hemorrhages, the GCS has been shown to be a predictor of outcome.[5]
However, clear consensus does not exist regarding many patients who fall between these extremes. Variation in surgical treatment exists even within a geographic region.
Indications for surgery in cerebellar hemorrhage (CH) remain controversial.[14]
Ventriculostomy may be indicated in patients with hemorrhage and hydrocephalus but is controversial as well, and is not recommended as an alternative to surgical evacuation as it may in turn be harmful.[14, 13]
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,[15, 16] but a specific size recommendation is lacking in more recent recommendations.[14, 16]
Patients with a large central clot and absent brainstem reflexes have a poor prognosis. In these cases, some advocate supportive therapy only.
Minimally Invasive Surgery (MIS) has shown some promise as an alternative to conventional surgical manuevers in small case series, but further studies are warranted.[17, 18, 19]
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.[20]
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.[21, 22, 23, 24]
Endoscopic hematoma evacuation has also been reported to have been effective in a small number of patients.
A large meta-analysis comparing surgical and medical treatment for CHs did not find improved functional outcomes with surgical hematoma evaluation, and showed that patients with smaller hematomas may have worse outcomes with surgical treatment. This reflects a continuing need for better identification of variables that might affect outcomes with surgical care and appropriate patient selection for these therapies.[25]
Patients with acute cerebellar hemorrhage (CH) should be monitored closely in a critical care setting, with consulting neurologists available.
It is reasonable to 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 are strongly recommended.
No specific drug therapy exists for cerebellar hemorrhage (CH). Medications useful in treating hypertension (eg, labetalol, nicardipine, clevidipine) 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 such as prothrombin complex concentrate that are specific for the coagulopathy. In patients with direct oral anticoagulant (DOAC)–induced coagulopathy, treatment with the specific antidote is recommended. There is great heterogeneity in clinical practice for treatment of patients with intracerebral hemorrhage regarding management of blood pressure, 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 from the principles and guidelines that guide treatment of intracerebral hemorrhage. For patients on antiplatelet therapy, transfusion of platelets or treatment with desomopressin (DDVAP) may be considered but are not routinely recommended.[26] Further study is needed.
Sonal Mehta, MD, Advanced Neuroscience Network Physicians, Steward Medical Group
Disclosure: Nothing to disclose.
Specialty Editors
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
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
Draga Jichici, MD, FRCPC, FAHA, Associate Clinical Professor, Division of Medicine, Department of Critical Care Medicine and Neurology, Co-Director, Neurosurgical Intensive Care Unit, Co-Director, Transcranial Doppler Ultrasound, Hamilton Health Sciences, McMaster University School of Medicine, Canada
Disclosure: Nothing to disclose.
J Stephen Huff, MD, FACEP, Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine
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