Left Cerebellar Stroke: Clinical Manifestations
Left cerebellar stroke typically presents with a triad of vertigo, headache, and gait imbalance, along with ipsilateral limb dysmetria and ataxia, but the most critical concern is monitoring for life-threatening brainstem compression and hydrocephalus that can develop within 12-72 hours. 1, 2
Initial Clinical Presentation
Common Symptoms
- Dizziness and vertigo are the most frequent initial complaints, often severe and rotatory in nature 1, 2
- Nausea and vomiting occur commonly, particularly with posterior inferior cerebellar artery (PICA) territory involvement 3, 1
- Headache is present in approximately 25% of cases and is part of the classic triad 3, 2
- Unsteady gait and difficulty with coordination are hallmark features 1, 4
- Dysarthria (speech disturbances) may be present 1, 5
Specific Neurological Findings on Examination
- Ipsilateral limb dysmetria (incoordination on the left side for left cerebellar stroke) 5, 2
- Ipsilateral axial lateropulsion (tendency to fall toward the left side) 5
- Truncal ataxia - frequently missed during bedside examination but critical to assess 1
- Abnormal eye movements requiring detailed examination 1
- Hearing loss may occur, particularly with anterior inferior cerebellar artery (AICA) infarction 1
- Intractable hiccups can be seen with PICA territory infarction 1
Level of Consciousness
Most patients are initially alert, though those with major cerebellar strokes can present with decreased consciousness due to brainstem compression or hydrocephalus 3, 1
Critical Warning Signs of Deterioration
Progressive impairment of consciousness is the single most reliable clinical indicator of tissue swelling and impending catastrophe. 6, 1
Early Warning Signs (12-72 hours post-onset)
- Declining level of arousal - monitor Glasgow Coma Scale; deterioration defined as GCS <12 on admission or decline ≥2 points 1
- Development of diplopia or new cranial nerve palsies from brainstem compression 6, 1
- Progressive ataxia beyond initial presentation 7
Late Signs (Immediately Before Herniation)
- Hypertension and bradycardia (Cushing's triad) 6
- Irregular breathing patterns and cardiac dysrhythmias 1
- Pupillary abnormalities: anisocoria or pinpoint pupils 1
- Loss of oculocephalic responses 1
Diagnostic Challenges and Pitfalls
Imaging Limitations
Initial CT can be normal in up to 25% of patients with cerebellar infarction, making clinical examination paramount 1, 4
Radiological Predictors of Dangerous Swelling
- Hypodensity involving >2/3 of the cerebellar hemisphere predicts space-occupying edema 6
- Compression or displacement of the 4th ventricle indicates brainstem compression 6, 1
- Evidence of hydrocephalus from fourth ventricular obstruction 1
Common Examination Errors
- Truncal ataxia is frequently missed during bedside examination - patients must be observed attempting to sit and walk 1
- Insufficient attention to coordination, gait, and eye movements leads to misdiagnosis 4
Initial Management Algorithm
Immediate Actions (Within Hours of Presentation)
All patients with cerebellar infarction must be evaluated immediately in a stroke unit by both a neurologist and neurosurgeon, with a precise management plan defined as soon as possible. 6, 7
Obtain rapid focused history and neurological examination to identify the pattern of presentation 7
Perform non-contrast head CT immediately to detect hemorrhage, mass effect, and hydrocephalus 7
Admit to intermediate or intensive care stroke unit for close neurological monitoring 6, 1
Monitoring Protocol (Up to 5 Days)
Even initially stable patients with territorial cerebellar infarctions require monitoring for up to 5 days, as peak swelling typically occurs 3-5 days after stroke onset 3, 6, 1
- Monitor level of arousal and pupillary function frequently to detect deterioration from cerebral swelling 1, 7
- Watch for new brainstem signs including cranial nerve palsies, breathing irregularities 1
- Serial neurological assessments for declining GCS or development of new deficits 1
Medical Management
- Mild fluid restriction - avoid hypo-osmolar fluids like 5% dextrose in water which may worsen edema 3
- Elevate head of bed 20-30 degrees to help venous drainage 3
- Treat factors that exacerbate raised intracranial pressure: hypoxia, hypercarbia, hyperthermia 3
- Avoid antihypertensive agents that induce cerebral vasodilation, as elevated blood pressure may be compensatory to maintain cerebral perfusion 3
- Osmotic therapy is reasonable for clinical deterioration but not for routine prophylaxis 7
Surgical Intervention Criteria
Surgical decompression is necessary when significant mass effect causes brainstem compression or obstructive hydrocephalus. 6, 7
- Do not wait for late signs of brainstem compression, as these appear immediately before herniation and respiratory arrest 7
- Advanced brainstem dysfunction is the only known predictor of unfavorable outcome in cerebellar infarctions 6, 7
- Delayed intervention >24 hours after symptom onset may predict unfavorable outcome 7
- Patients in coma after hydrocephalus may benefit from aggressive surgical treatment as long as conditions are reversible 8
Prevention of Subacute Complications
- Subcutaneous anticoagulants or intermittent external compression stockings to prevent deep vein thrombosis among immobilized patients 3
- Early mobilization when safe 3
- Measures to prevent aspiration, pneumonia, pressure sores, and contractures 3
- Antibiotics for infectious complications 3
Vascular Territory Differences
PICA (Posterior Inferior Cerebellar Artery) Territory
- More severe vertigo (rotatory) predominates 5, 2
- Higher risk of complications: 30% develop severe mass effect, 19% develop hydrocephalus requiring intervention 2
- Four deaths occurred in one series from brainstem compression 2