How should a cerebellar lesion be evaluated and managed?

Evaluation and Management of Cerebellar Lesions

Patients with cerebellar lesions require immediate neuroimaging with MRI (preferred) or CT, urgent neurosurgical consultation, and close monitoring in a stroke unit or ICU, with surgical evacuation indicated for hemorrhages ≥3 cm or any lesion causing brainstem compression, hydrocephalus, or neurological deterioration. 1, 2

Initial Assessment and Risk Stratification

Clinical Presentation Patterns

Cerebellar infarction typically presents with:

• Vertigo, headache, and gait imbalance (especially in posterior inferior cerebellar artery territory) 3
• Progressive ataxia, dysarthria, and limb dysmetria 1
• Nausea, vomiting, and diplopia 1
• Critical warning signs: Progressive impairment of consciousness, cranial nerve palsies, pyramidal signs 1

Cerebellar hemorrhage presents similarly but with higher risk of rapid deterioration:

• Symptoms range from mild stroke-like presentation to catastrophic decline 4
• The posterior fossa's tight compartment tolerates minimal additional volume 4

High-Risk Features Requiring Immediate Action

Clinical predictors of space-occupying edema 1:

• Impairment of consciousness
• Signs of brainstem compression: hypertension, bradycardia, progressive reduction of consciousness (appear late before herniation) 1

Radiological predictors demanding urgent intervention 1:

• Hypodensity involving ≥2/3 of cerebellar hemisphere
• Compression or displacement of fourth ventricle
• Obstructive hydrocephalus
• Brainstem displacement
• Compression of basal cisterns
• Hemorrhagic transformation

Immediate Management Protocol

Step 1: Stabilization and Monitoring (First 24-72 Hours)

All patients with risk factors must be evaluated immediately by both neurology and neurosurgery 1. A precise management plan should be defined on admission, as delayed intervention causes irreversible harm 1.

General measures 1:

• Close neurological and cardiovascular monitoring in stroke unit or ICU (up to 5 days for territorial cerebellar infarctions, even if stable) 1
• Elevate head of bed 0-30° during periods of increased ICP 1, 5
• Ensure cerebral oxygenation >94% 1
• Avoid hypo-osmolar fluids 1, 5
• Treat hyperthermia (>37.5°C), hyperglycemia (>8 mmol/L), and hypercarbia aggressively 1, 5
• NPO status 1
• Correct hypovolemia with isotonic fluids 1

Antiplatelet management: Withhold if craniectomy likely; if surgery ruled out, give aspirin 100-300 mg 1

Step 2: Imaging Strategy

MRI is the preferred initial imaging modality for cerebellar lesions 1. MRI provides superior soft tissue contrast for detecting:

• Parenchymal volume loss
• Signal intensity alterations
• Early ischemic changes not visible on CT 6

CT head without contrast is acceptable when MRI unavailable but has inferior sensitivity for early cerebellar infarction 6. CT is useful for detecting hemorrhage and calcification 1.

Step 3: Surgical Decision-Making

For Cerebellar Hemorrhage

Immediate surgical evacuation (Class I, Level B-NR) is indicated for 1, 2:

• Neurological deterioration
• Brainstem compression
• Hydrocephalus from ventricular obstruction
• Cerebellar ICH volume ≥15 mL (or ≥3 cm diameter) 1, 2

Critical pitfall: External ventricular drainage (EVD) alone is potentially harmful and insufficient when brainstem compression exists 1, 2. Surgery reduces mortality in cerebellar hemorrhage 2.

Surgical approach: Suboccipital craniotomy with decompression and hematoma evacuation 5. Ventriculostomy may serve as bridge to definitive surgery but should not replace it 5.

For Cerebellar Infarction

Surgical decompression indicated for 1:

• Progressive neurological deterioration despite medical management
• Radiographic evidence of significant mass effect with brainstem compression
• Obstructive hydrocephalus
• Infarction involving >1/3 of cerebellar hemisphere 5

Timing considerations: Intervention within 24 hours of symptom onset may prevent irreversible harm, though delayed intervention >24 hours may predict worse outcomes 1. The only known predictor of unfavorable outcome is advanced brainstem dysfunction (e.g., locked-in syndrome) 1.

Observation vs. Immediate Surgery

For large cerebellar lesions (>3 cm/15 mL) in patients with good clinical condition, initial conservative management with close monitoring is reasonable 1. However, maintain low threshold for surgical intervention if any deterioration occurs.

Posterior inferior cerebellar artery (PICA) territory infarcts carry 30% risk of severe mass effect and 19% risk of fatal brainstem compression, requiring more aggressive monitoring than superior cerebellar artery (SCA) infarcts (7% risk) 3.

Etiology-Specific Considerations

Ischemic Stroke

• Cardioembolism is the most common mechanism for territorial cerebellar infarcts 7, 3
• Consider thrombolysis and endovascular interventions for eligible patients 5
• Vertebral artery dissection and atherosclerotic disease are important causes 7

Hemorrhage

• Reverse coagulopathy immediately with prothrombin complex concentrate or fresh frozen plasma 8
• Control blood pressure to systolic <160 mmHg 9

Tumor

• Use steroids for vasogenic edema (not indicated for cerebrovascular disease) 5
• Consider radiotherapy/chemotherapy as appropriate 5

Common Pitfalls to Avoid

1. Misdiagnosis due to nonspecific symptoms: Cerebellar stroke often presents with dizziness, nausea, vomiting—symptoms easily attributed to benign causes 6. Always perform careful coordination, gait, and eye movement examination 6.

2. Over-reliance on early CT: Early posterior fossa ischemia is rarely seen on CT 6. Use MRI when cerebellar stroke suspected.

3. Delayed neurosurgical consultation: Contact neurosurgery immediately upon diagnosis 1. The goal is intervention within hours when indicated.

4. Using EVD alone for cerebellar hemorrhage with brainstem compression: This is insufficient and potentially harmful 1, 2.

5. Inadequate monitoring duration: Even stable-appearing patients with territorial cerebellar infarction require up to 5 days of close monitoring 1.