For bilateral corona radiata infarcts, should they be classified as a lacunar infarct (LACI) or a partial anterior circulation infarct (PACI)?

Classification of Bilateral Corona Radiata Infarcts

Bilateral corona radiata infarcts should be classified as LACI (lacunar infarcts) if they meet size criteria (<1.5 cm), are confined to subcortical white matter, and present without cortical signs—the bilateral nature does not automatically change their classification to PACI. 1, 2

Diagnostic Criteria for Lacunar Classification

The classification hinges on three essential elements that must all be satisfied:

Imaging Requirements

• Each individual infarct must measure <1.5 cm in diameter on CT or MRI 1, 3
• Lesions should be confined to deep white matter (corona radiata) without cortical involvement 1
• The term "lacunar infarct" is most appropriately reserved for cystic lesions <1 cm in the basal ganglia, brainstem, or deep white matter 1

Clinical Presentation Must Lack Cortical Signs

• The defining characteristic is the absence of cortical dysfunction—no aphasia, no neglect, no visual field defects 1, 2
• Patients should present with classical lacunar syndromes: pure motor hemiparesis, pure sensory syndrome, sensorimotor stroke, ataxic hemiparesis, or dysarthria-clumsy hand 1, 4
• The presence of aphasia or other cortical signs would mandate PACI classification regardless of infarct size 2

Exclusion of Alternative Mechanisms

• You must exclude ipsilateral large-artery stenosis >50% through carotid imaging (duplex ultrasound, CTA, or MRA) 1, 3
• Cardiac evaluation with transthoracic echocardiography and extended rhythm monitoring is mandatory to exclude cardioembolic sources 3
• If atrial fibrillation or another cardioembolic source is identified, the patient requires anticoagulation regardless of small infarct size—this is a critical therapeutic distinction 3, 2

Special Considerations for Bilateral Infarcts

Clinical Patterns in Bilateral Corona Radiata Disease

• Bilateral multiple corona radiata infarcts frequently present with bilateral motor and sensory symptoms plus neuropsychological deficits 5
• Approximately 25% of corona radiata infarct patients have bilateral involvement, and these patients more commonly show complete sensorimotor deficits 5
• Dysarthria occurs in 25% of cases but has no localizing value for unilateral versus bilateral disease 5

Underlying Pathophysiology

• Small-artery disease with long-standing hypertension accounts for 59% of corona radiata infarcts, making it the dominant mechanism 5
• Leukoaraiosis (white matter hyperintensities) is present in 88% of patients with corona radiata infarcts and is significantly more frequent in those with bilateral multiple infarcts compared to unilateral single infarcts 5
• This coexistence suggests a shared pathophysiological mechanism of chronic small vessel disease 5

Critical Diagnostic Pitfall

Clinical classification alone is notoriously unreliable for distinguishing lacunar from small cortical infarcts. 6

• In a prospective MRI study, OCSP clinical classification correctly identified only 39% of lacunar infarcts, with a positive predictive value of just 39% 6
• 61% of patients clinically classified as LACI actually had radiographic appearances consistent with PACI (small cortical infarcts) 6
• Conversely, 15% of those classified as PACI had true lacunar infarcts 6
• MRI with diffusion-weighted imaging is therefore mandatory for accurate classification—clinical syndrome alone is insufficient 3, 6

Algorithmic Approach to Classification

1. Obtain MRI (superior to CT) to confirm infarct location, size, and number 3, 2
2. Measure each lesion: Are all infarcts <1.5 cm and confined to subcortical white matter? 1
3. Assess clinical presentation: Are cortical signs (aphasia, neglect, visual field defects) absent? 1, 2
4. Complete vascular workup: Exclude >50% large-artery stenosis with carotid imaging 1, 3
5. Perform cardiac evaluation: TTE and rhythm monitoring to exclude cardioembolic sources 3
6. If all criteria met: Classify as LACI despite bilateral distribution 1, 5
7. If cortical signs present or cardioembolic source identified: Reclassify and adjust treatment accordingly 3, 2

Management Implications

• For confirmed bilateral lacunar infarcts: Antiplatelet therapy, aggressive blood pressure control (target <130 mmHg systolic), statin therapy, and risk factor modification 1, 3, 4
• If misclassified and cardioembolic source exists: Anticoagulation is required, not just antiplatelet therapy 3, 2
• Bilateral involvement with leukoaraiosis signals higher risk for vascular cognitive impairment (develops in ~20% after first lacunar stroke and >33% with recurrent events) 1, 5