Management of Cerebellar Infarct with Vertebral Artery Dissection
For acute cerebellar infarction caused by vertebral artery dissection, initiate immediate anticoagulation with intravenous heparin (targeting PTT 1.5-2.0 times control) or low molecular weight heparin, followed by warfarin (target INR 2.0-3.0) for 3-6 months, then transition to antiplatelet therapy; simultaneously arrange urgent neurosurgical consultation and intensive care monitoring for signs of cerebellar edema requiring decompressive suboccipital craniectomy. 1, 2
Immediate Diagnostic Confirmation
- Obtain contrast-enhanced CTA or MRA urgently to confirm vertebral artery dissection, as these modalities have largely supplanted catheter angiography for diagnosis. 1
- Brain MRI is superior to CT for detecting acute cerebellar infarction, particularly in the first 24-48 hours when CT may appear normal. 3
- Carotid duplex ultrasonography may miss dissections beginning above the angle of the mandible; contrast-enhanced CTA and MRA are superior in these cases. 1
Critical Triage and Monitoring
Transfer immediately to intensive care or stroke unit with neurosurgical consultation, even if the patient appears stable initially, as deterioration can occur rapidly. 2, 4
Neurological Monitoring Parameters
- Monitor frequently for signs of cerebellar swelling and brainstem compression: declining level of consciousness, pupillary changes, loss of oculocephalic responses, and new brainstem signs. 2
- Obtain serial CT scans in the first 48 hours to identify patients developing symptomatic swelling before clinical deterioration becomes irreversible. 2
- Drowsiness or declining consciousness in bilateral cerebellar infarcts represents a neurosurgical emergency requiring immediate intervention. 4
Antithrombotic Therapy (Primary Treatment)
Anticoagulation is the cornerstone of treatment for symptomatic vertebral artery dissection (Class IIa recommendation). 1, 5
Anticoagulation Regimen Options
- Intravenous heparin: Dose-adjusted to prolong PTT to 1.5-2.0 times control, followed by warfarin (target INR 2.5, range 2.0-3.0) for 3-6 months. 1
- Low molecular weight heparin: Use dosing recommended for venous thromboembolism, followed by warfarin (target INR 2.5, range 2.0-3.0) for 3-6 months. 1
- Direct oral anticoagulation: May be initiated without antecedent heparin in select cases. 1
Transition to Antiplatelet Therapy
- After 3-6 months of anticoagulation, transition to aspirin (81-325 mg daily) or clopidogrel (75 mg daily) for long-term secondary prevention. 1, 5
- The prognosis is usually favorable with appropriate antithrombotic therapy. 1, 5
Critical Anticoagulation Caveat
Do not anticoagulate if there is concern for intracranial extension of dissection with subarachnoid hemorrhage risk, as anticoagulation may adversely influence outcomes in this scenario. 1, 5
Medical Management of Cerebellar Edema
Supportive Care Measures
- Elevate head of bed 0-30 degrees to help control intracranial pressure. 2
- Maintain isotonic fluid resuscitation only—avoid hypotonic fluids and dextrose-containing solutions to ensure adequate cerebral perfusion. 2, 4
- Maintain normoglycemia and treat hyperthermia aggressively. 2
- Provide supplemental oxygen for at least 24 hours. 2
Osmotic Therapy
- Administer mannitol or hypertonic saline for patients with clinical deterioration from cerebral edema (Class IIa recommendation). 2
- Monitor serum osmolality at regular intervals with target of 300-310 mOsmol/kg when using osmotic therapy. 2
Blood Pressure Management
- Maintain systolic BP <220 mmHg and diastolic <120 mmHg in the acute setting to preserve cerebral perfusion while avoiding hemorrhagic transformation. 4
- Avoid aggressive blood pressure lowering, as hypertension may be compensatory to maintain cerebral perfusion pressure in the setting of brainstem compression. 4
- Maintain cerebral perfusion pressure >60 mmHg using volume replacement and/or catecholamines if necessary. 2
Medications to Avoid
Do not use corticosteroids, barbiturates, or hypothermia for cerebellar edema—there is insufficient evidence and they are not recommended (Class III recommendation). 2
Surgical Intervention
Indications for Suboccipital Craniectomy
Perform suboccipital craniectomy with dural expansion in patients with cerebellar infarctions who deteriorate neurologically despite maximal medical therapy (Class I recommendation, Level of Evidence B). 2
Specific Surgical Triggers
- Declining level of consciousness (drowsiness progressing to stupor). 2, 4
- Radiographic signs of mass effect: fourth ventricular compression, hydrocephalus, or brainstem compression. 2, 6
- Clinical signs of brainstem compression: pupillary changes, loss of brainstem reflexes, respiratory irregularities. 2
Critical Surgical Pitfall
Do not perform ventriculostomy alone without decompressive craniectomy, as this can cause fatal upward herniation through the tentorial notch. 2, 4
- While some patients with hydrocephalus and preserved consciousness may initially respond to external ventricular drainage alone, those with declining consciousness require definitive decompression. 6
- Reserve external ventricular drainage for patients with worsening consciousness and radiologically evident ventricular enlargement who have not yet developed signs of direct brainstem compression. 6
Endovascular Intervention for Dissection
Carotid angioplasty and stenting might be considered when ischemic neurological symptoms persist or recur despite antithrombotic therapy (Class IIb recommendation). 1
- Surgical revascularization techniques include direct repair and resection with vein graft replacement, but are rarely needed. 1
- Endovascular stent angioplasty has been successful in small case series but carries complication risks. 1
- One case report describes successful embolization of the affected vertebral artery to prevent further distal embolism when anticoagulation failed. 7
Long-Term Medical Management
Statin Therapy
Initiate high-intensity statin therapy to reduce LDL cholesterol to <70 mg/dL (Class I recommendation for extracranial vertebral artery disease; Class IIa for post-stroke patients). 5
- Statins provide benefits beyond cholesterol reduction: endothelial stabilization, increased nitric oxide bioavailability, reduced oxidative stress, and decreased vascular inflammation. 5
- For patients intolerant to statins, use bile acid sequestrants and/or niacin (Class IIa recommendation). 5
Blood Pressure Control
- The safety and effectiveness of specific antihypertensive agents (β-blockers, ACE inhibitors, non-dihydropyridine calcium channel blockers) to reduce arterial wall stress are not well established (Class IIb recommendation). 1
- However, long-term blood pressure control to normal range is reasonable to prevent recurrence. 1
Lifestyle Modifications
- Smoking cessation (Class I recommendation). 5
- Diet and exercise modifications, particularly for patients with diabetes mellitus. 5
Follow-Up Imaging
Serial non-invasive imaging of the extracranial vertebral arteries is reasonable to assess disease progression and exclude development of new lesions (Class IIa recommendation). 5
Common Pitfalls to Avoid
- Delaying neurosurgical consultation is the most critical error—involve neurosurgery early even if the patient appears stable, as deterioration can be rapid and irreversible. 2, 4
- Relying on initial CT scan alone—normal CT does not exclude cerebellar infarction; obtain MRI if clinical suspicion is high. 3
- Using hypoosmolar fluids—maintain isotonic or mildly hypertonic solutions only. 2, 4
- Minimizing sedation excessively—avoid medications that impair consciousness assessment to allow accurate neurological monitoring. 2
- Performing ventriculostomy without craniectomy in patients with declining consciousness—this risks upward herniation. 2, 4
- Ignoring cardiac monitoring—arrhythmias are common after cerebellar infarcts compressing the brainstem. 2
DVT Prophylaxis
Initiate DVT prophylaxis with subcutaneous low-dose heparin or low molecular weight heparin once it is safe to do so, typically after consulting neurosurgery if surgical intervention has occurred. 2