What is the appropriate management for a patient with a left posterior cerebral artery (PCA) territory acute or subacute infarct of the occipital lobe and evidence of intraparenchymal microhemorrhage, presenting with inferior right homonymous quadrantanopsia?

Management of Left PCA Territory Infarct with Microhemorrhage

In this patient with a subacute left PCA territory occipital infarct and intraparenchymal microhemorrhage presenting 2 weeks after symptom onset, initiate antiplatelet therapy with aspirin 81-325 mg daily as the primary treatment, while avoiding anticoagulation due to the presence of microhemorrhage. 1

Antiplatelet Therapy Selection

The presence of microhemorrhage is a critical contraindication to anticoagulation, making antiplatelet therapy the appropriate choice for secondary stroke prevention. 1

• Aspirin (81-325 mg daily) is the recommended first-line antiplatelet agent for patients with ischemic stroke in the posterior circulation territory. 1
• Alternative antiplatelet options include clopidogrel 75 mg daily or the combination of aspirin plus extended-release dipyridamole (25/200 mg twice daily) if aspirin is contraindicated or not tolerated. 1
• Dual antiplatelet therapy (aspirin plus clopidogrel) is NOT indicated in this case, as it is only recommended for minor strokes when initiated within 24 hours of symptom onset for up to 90 days. 1 This patient presented at 2 weeks, well beyond the therapeutic window for dual antiplatelet therapy.

Why Anticoagulation is Contraindicated

The presence of intraparenchymal microhemorrhage represents an absolute contraindication to anticoagulation therapy, even though the PCA appears patent. 1

• While anticoagulation for 3-6 months is typically considered for patients with acute vertebrobasilar territory ischemia and angiographic evidence of thrombus in the extracranial vertebral artery, the microhemorrhage in this case overrides this consideration. 1
• The risk of hemorrhagic expansion with anticoagulation outweighs any potential benefit in preventing recurrent embolism. 1

Comprehensive Vascular Workup Required

Despite the 2-week delay, a thorough evaluation for stroke mechanism is essential to guide long-term secondary prevention. 2

• Obtain echocardiography (preferably transesophageal) to evaluate for cardioembolic sources, as cardiac embolism is the most common mechanism of PCA territory infarction. 2
• Perform carotid and vertebral artery duplex ultrasound or CTA/MRA to assess for atherosclerotic disease, as vertebrobasilar atheroma with local embolism is another common mechanism. 1, 2
• Evaluate for atrial fibrillation with prolonged cardiac monitoring (at least 24 hours), as this would significantly alter long-term management once the microhemorrhage has resolved. 1
• Consider hypercoagulable workup in younger patients or those without traditional vascular risk factors. 2

Risk Factor Modification

Aggressive cardiovascular risk factor management is as important as antiplatelet therapy for preventing recurrent stroke. 1

• Initiate high-intensity statin therapy regardless of baseline lipid levels for all patients with ischemic stroke. 1
• Target blood pressure control with antihypertensive medications, aiming for <140/90 mmHg in most patients. 1
• Address modifiable risk factors including smoking cessation, diabetes management, and lifestyle modifications. 1

Monitoring and Follow-up Imaging

Serial neuroimaging is reasonable to monitor for hemorrhagic transformation and resolution of microhemorrhage. 1

• Repeat MRI with gradient-echo sequences at 3-6 months to reassess the microhemorrhage burden. 3
• If microhemorrhages have resolved and a high-risk cardioembolic source (such as atrial fibrillation) is identified, anticoagulation may be reconsidered at that time, though this decision requires careful risk-benefit analysis. 1
• Annual noninvasive imaging of vertebral and carotid arteries is reasonable to assess for progression of atherosclerotic disease. 1

Critical Management Pitfalls to Avoid

Do not initiate anticoagulation in the presence of microhemorrhage, even if a cardioembolic source is identified. 1 The hemorrhagic risk outweighs the benefit in the acute/subacute phase.

Do not delay antiplatelet therapy beyond the acute phase. 1 While aspirin should be held for 24 hours after thrombolysis, this patient is 2 weeks out and should already be on antiplatelet therapy.

Do not assume the stroke mechanism without comprehensive workup. 2 PCA territory infarctions have heterogeneous etiologies including cardiac embolism, vertebrobasilar atheroma, migraine-related mechanisms, and coagulopathy, each requiring different long-term management strategies.

Do not overlook the possibility of anomalous vascular anatomy. 4 Persistent embryonic connections between carotid and basilar circulations can result in posterior circulation infarcts from carotid disease, which would alter surgical management considerations.

Prognosis and Rehabilitation

Visual field defects from occipital infarction may show remarkable recovery over extended periods, particularly with active rehabilitation. 5

• Refer for neuro-ophthalmology evaluation and visual rehabilitation strategies. 6, 5
• Neuropsychological testing may be warranted if cognitive complaints emerge, as occipito-temporal infarcts can cause topographical disorientation, memory problems, and executive dysfunction beyond the visual field defect. 5
• Neuroplastic changes can occur over years, supporting continued rehabilitation efforts even when initial recovery plateaus. 5