What are the differential diagnoses for an 11-year-old male with an acute ischemic infarct of the left thalamus and left cerebellopontine region with hemorrhagic conversion presenting with isolated left facial nerve palsy?

Differential Diagnoses for Stroke in an 11-Year-Old with Thalamic and Cerebellopontine Infarction with Hemorrhagic Conversion

The most critical next step is to aggressively investigate for infectious vasculitis—particularly neuroborreliosis—and cardiac sources of embolism including infective endocarditis, as these are the leading treatable causes of pediatric stroke with hemorrhagic transformation. 1, 2

Primary Differential Diagnoses to Investigate

1. Infectious Vasculitis (Highest Priority)

Neuroborreliosis is emerging as a leading cause of pediatric stroke with secondary vasculitis and should be tested immediately in any child with stroke, especially with the prodrome of headache and vomiting. 1

• A 13-year-old with neuroborreliosis presented with identical features: thalamic infarction, recurrent headaches, and facial nerve palsy. 1
• Test both serum and CSF for Borrelia burgdorferi antibodies (IgG and IgM), as positive IgG alone does not exclude active disease. 1
• The six-month prodrome of headache and vomiting in your patient strongly suggests an indolent infectious or inflammatory process. 1
• Empiric treatment with third-generation cephalosporin (ceftriaxone 2g IV daily for 14-28 days) should be considered while awaiting results if clinical suspicion is high. 1

2. Infective Endocarditis (Critical to Exclude)

Infective endocarditis must be ruled out urgently given the hemorrhagic conversion, which occurs in only 2% of modern IE-related strokes but carries devastating consequences. 2

• Order transthoracic echocardiogram immediately, followed by transesophageal echocardiogram (TEE) if initial study is negative, as TEE changes management in 16-20% of suspected cardioembolic strokes. 2
• Check C-reactive protein: a level ≥10 mg/L increases the likelihood of IE by 22-fold (OR 22). 2
• Obtain three sets of blood cultures before any antibiotics. 2
• The vomiting episodes may represent septic emboli or increased intracranial pressure from the hemorrhagic conversion. 2

3. Cardiac Structural Abnormalities

Patent foramen ovale (PFO) with paradoxical embolism is a common cause of cryptogenic stroke in young patients. 2

• TEE is superior to transthoracic echo for detecting PFO and should be performed if initial workup is negative. 2
• Cardiac CT or MRI may reveal additional structural abnormalities in 52% of young stroke patients and changes management in 16%. 2
• Look for evidence of deep vein thrombosis as a source of paradoxical embolus. 2

4. Hypercoagulable States

Test for inherited thrombophilias, though yield is lower in children >10 years compared to younger children. 2

• Order: protein C, protein S, antithrombin III, factor V Leiden, prothrombin G20210A mutation, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-β2-glycoprotein I). 2
• Check homocysteine and lipoprotein(a) levels. 2
• Monogenic causes are detected in 7% of population-based stroke studies when systematic algorithms are used. 2

5. Arteriopathy/Vasculopathy

Intracranial arteriopathy including moyamoya disease, arterial dissection, or vasculitis must be considered. 2

• Your CT angiogram showed no aneurysm or malformation, but repeat with MR angiography for superior visualization of vessel wall abnormalities and small-vessel disease. 2
• MRA and CTA reliably exclude high-grade intracranial atherosclerotic stenosis when negative. 2
• Consider conventional catheter angiography if MRA/CTA are inconclusive, as it remains the gold standard for detecting subtle vasculopathy. 2

6. Drug-Induced Stroke

Toxicology screening for cocaine and amphetamines is mandatory, as cocaine use increases stroke risk >6-fold in young adults. 2

• Obtain urine drug screen immediately, even with negative history, as adolescents may not disclose substance use. 2

Management Algorithm

Immediate Actions (Next 24-48 Hours)

1. Infectious workup:

   • Blood cultures × 3 2
   • Serum and CSF Borrelia antibodies 1
   • C-reactive protein, ESR, complete blood count with differential 2
   • Consider empiric ceftriaxone if high suspicion for neuroborreliosis 1

2. Cardiac evaluation:

   • Transthoracic echocardiogram stat 2
   • TEE if TTE negative or inadequate 2
   • Extended cardiac monitoring (≥24 hours) for paroxysmal atrial fibrillation 3

3. Vascular imaging:

   • MRI brain with diffusion-weighted imaging (DWI) and MR angiography of head and neck 4, 3
   • Consider conventional angiography if MRA inconclusive 2

4. Hematologic workup:

   • Hypercoagulable panel 2
   • Urine toxicology screen 2

Monitoring for Hemorrhagic Expansion

The hemorrhagic conversion significantly impacts anticoagulation decisions and prognosis. 2

• Hemorrhagic transformation occurs in 38-71% of all strokes at autopsy but is symptomatic in only 0.6-20%. 2
• Repeat head CT in 24-72 hours to assess for expansion of hemorrhage before considering any anticoagulation. 2
• Large infarcts (entire vascular territory) have nearly twice the risk of hemorrhagic transformation. 2
• The thalamic location (4.6% of IE strokes) has better neurological recovery than middle cerebral artery territory (50% vs 83% complete recovery). 2

Critical Pitfalls to Avoid

• Do not attribute isolated facial palsy to Bell's palsy in the setting of known stroke—this represents pontine involvement at the facial nerve nucleus/fascicle. 5, 4
• Do not delay infectious workup while pursuing other etiologies—neuroborreliosis and IE are immediately treatable causes. 1, 2
• Do not start anticoagulation until hemorrhagic transformation is stable and cardiac source is confirmed, as this increases mortality. 2, 6
• Do not assume negative initial imaging excludes stroke—small pontine infarcts can be as small as 4mm and are easily missed on CT. 5, 4

Prognosis Considerations

Younger patients with decreased intracranial compliance are at increased risk for brain tissue shift from edema, which peaks several days after infarction. 2

• Early nausea and vomiting (present in your patient) are associated with increased cerebral edema after large stroke. 2
• The current clinical stability (GCS 15, ambulatory) is reassuring but does not exclude delayed deterioration. 2
• Neurological deterioration occurs in approximately 25% of acute stroke patients and requires close monitoring. 3