What is the recommended workup for a patient with multiple remote cerebellar thromboembolic infarcts?

Recommended Workup for Multiple Remote Cerebellar Thromboembolic Infarcts

For patients with multiple remote cerebellar thromboembolic infarcts, perform comprehensive vascular imaging with CTA or MRA of head and neck, cardiac evaluation including transthoracic echocardiography with bubble study (or transesophageal echocardiography if higher yield suspected), prolonged cardiac monitoring for atrial fibrillation, and hypercoagulability testing particularly in younger patients without obvious risk factors. 1, 2

Initial Brain Imaging Assessment

• MRI head without IV contrast is the preferred modality for characterizing the extent, age, and distribution of cerebellar infarcts, as it provides superior detection of small and multiple ischemic lesions compared to CT 1
• CT head without IV contrast is an acceptable alternative if MRI is contraindicated, though it has lower sensitivity for small cerebellar lesions 1
• The imaging helps distinguish territorial versus non-territorial (border zone) patterns, which provides clues to mechanism—territorial infarcts suggest embolic etiology while border zone patterns may indicate hemodynamic compromise 3, 4

Vascular Imaging to Identify Embolic Sources

CTA head and neck or MRA head and neck without IV contrast should be performed rapidly to evaluate for:

• Large artery atherosclerotic disease of the vertebrobasilar system, which is present in 19-23% of cerebellar infarcts and can cause artery-to-artery embolism 5, 4, 6
• Vertebral artery occlusive lesions, found in 60% of patients with multiple cerebellar infarcts 6
• Basilar artery stenosis or occlusion, which can lead to distal embolization 5, 4
• The pattern of multiple infarcts in different cerebellar artery territories (PICA, AICA, SCA) strongly suggests an embolic mechanism 5, 7, 6

CTA is usually appropriate as it provides rapid acquisition and excellent visualization of vessel anatomy 1

Cardiac Evaluation for Cardioembolic Sources

Transthoracic echocardiography with bubble study (agitated saline contrast) is essential because:

• Cardiac sources of embolism are identified in 23-42% of cerebellar infarcts 4, 6
• Multiple cerebellar infarcts have a 20% rate of cardiogenic embolism 6
• The bubble study screens for patent foramen ovale and intracardiac shunts 2

Transesophageal echocardiography should be considered if transthoracic echo is non-diagnostic and clinical suspicion remains high, as it provides superior visualization of left atrial appendage thrombus, atrial septal abnormalities, and aortic arch atheroma 2

Prolonged cardiac monitoring (minimum 30 days) is recommended to detect paroxysmal atrial fibrillation, which may not be evident on initial telemetry or 12-lead ECG 2

Hypercoagulability Testing

Obtain a comprehensive hypercoagulability panel, particularly in patients under 50 years or without traditional vascular risk factors, including:

• Protein C and Protein S levels 1
• Antithrombin III 1
• Factor V Leiden mutation 1
• Prothrombin gene mutation (G20210A) 1
• Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies, anti-beta-2-glycoprotein I) 1
• Homocysteine level 1
• MTHFR gene mutation 1

This is particularly important because hypercoagulable states occur in 17% of non-territorial cerebellar infarcts versus only 1.25% of territorial infarcts (odds ratio 15.6) 4

Additional Laboratory Evaluation

• Complete blood count to assess for polycythemia or thrombocytosis 2
• Comprehensive metabolic panel including renal and hepatic function 2
• Fasting lipid panel (LDL, HDL, triglycerides) 2
• Hemoglobin A1c for diabetes screening 2
• Inflammatory markers (ESR, CRP) if vasculitis is suspected based on age and clinical presentation 2

Clinical Context and Mechanism Determination

The distribution pattern provides critical mechanistic information:

• Multiple infarcts in different cerebellar artery territories (PICA + SCA, or PICA + AICA + SCA) strongly suggest embolic mechanism, either cardioembolic or artery-to-artery embolism 5, 7, 6
• Very small multiple infarcts (<2 cm) can be either embolic (territorial end-zone infarcts) or related to small vessel disease/hypercoagulable states 3, 4, 7
• Border zone infarcts suggest hemodynamic compromise from proximal large artery stenosis, particularly bilateral vertebral or basilar artery disease 3, 4
• The presence of concomitant vertebrobasilar occlusive disease with cardiac sources (found in 8% of cases) requires careful consideration of dual mechanisms 4

Common Pitfalls to Avoid

• Do not assume all small cerebellar infarcts are lacunar strokes—they have the same high rate of embolic mechanism (47%) as territorial infarcts and require full embolic workup 4
• Do not stop at identifying one potential cause—6-8% of patients have both large artery disease and cardiac sources, requiring dual antiplatelet and anticoagulation consideration 4
• Do not delay vascular imaging—artery-to-artery embolism from vertebrobasilar disease is the predominant mechanism (33-60%) and requires urgent identification for secondary prevention 5, 6
• Do not overlook the need for admission and monitoring—even remote infarcts require assessment for risk of recurrence, and any new symptoms warrant immediate re-evaluation 8

Secondary Prevention Considerations

Once the workup identifies the mechanism:

• For cardioembolic sources (especially atrial fibrillation): initiate direct oral anticoagulants as first-line therapy 2
• For atherosclerotic arterial disease: start dual antiplatelet therapy (aspirin plus clopidogrel) for 21-90 days, then transition to single agent, plus high-intensity statin regardless of baseline LDL 2
• Aggressive vascular risk factor modification with blood pressure target <130/80 mmHg, LDL <70 mg/dL, hemoglobin A1c <7%, smoking cessation, and 150 minutes weekly of moderate-intensity aerobic activity 2