Etiology of Lenticulostriate Artery Infarctions
Lenticulostriate infarctions are primarily caused by cardioembolism, not by hypertension-related small vessel disease (lipohyalinosis) as traditionally assumed. 1
Primary Mechanism: Embolism
Cardiac embolism is the principal mechanism for lenticulostriate infarction, contrary to the traditional concept that these infarcts result primarily from hypertensive lipohyalinosis. 1
In patients with lenticulostriate territory infarcts, embolic sources are identified in 35% of cases: 28% from large vessel atherosclerotic plaque and 15% from cardiac sources. 2
Even among patients with hypertension or diabetes mellitus (traditional small vessel disease risk factors), 36% have identifiable carotid or cardiac embolic sources. 3
Among patients without hypertension or diabetes, 32% still have possible carotid or cardiac etiology, further supporting embolism as a dominant mechanism. 3
Secondary Role: Hypertension and Small Vessel Disease
While hypertension is commonly present, it appears to be a contributing factor rather than the sole cause:
Hypertension is present in 68% of patients with lenticulostriate infarcts, and diabetes in 37%, but both conditions occur together in only 28%. 3
Notably, 23% of patients have neither hypertension nor diabetes, indicating that small vessel disease from these conditions cannot explain all cases. 3
The American Heart Association guidelines classify small-artery (lacunar) strokes as "generally associated with diabetes or hypertension" but explicitly state they are "not usually caused by atherosclerosis." 4, 5
Arteriosclerosis Considerations
Large artery atherosclerosis contributes through artery-to-artery embolism rather than direct occlusion of the lenticulostriate vessels themselves. 4
Hypertension causes both atherosclerosis of medium-large arteries and arteriolosclerosis of arterioles through mechanical and humoral endothelial damage. 6
Critical Clinical Implications
The concept of lacunar infarctions relating to lipohyalinosis is "perhaps too often proposed without evidence," and this misattribution has important therapeutic consequences. 1
Mandatory Diagnostic Workup
You must exclude embolic sources before attributing a lenticulostriate infarct to small vessel disease alone:
Cardiac evaluation is required: transthoracic echocardiography and extended rhythm monitoring to detect paroxysmal atrial fibrillation. 7
Carotid imaging within 48 hours (duplex ultrasound, CTA, or MRA) to exclude ipsilateral large-artery stenosis >50%. 7
Vascular imaging (CTA or MRA) must be obtained urgently to exclude large vessel occlusion, even when lacunar stroke is suspected clinically. 7
Treatment Depends on Mechanism
If atrial fibrillation or high-risk cardiac source is identified, anticoagulation is required regardless of small infarct size—not just antiplatelet therapy. 7, 5
If small vessel disease is confirmed after excluding embolic sources, use antiplatelet therapy with aggressive risk factor modification and blood pressure target <130 mmHg systolic. 7
Common Pitfall to Avoid
Do not assume hypertension alone explains a lenticulostriate infarct. The high incidence of carotid and cardiac disease in patients both with and without traditional small vessel disease risk factors mandates comprehensive evaluation for treatable embolic sources. 3 Misclassification leads to inappropriate treatment—missing an indication for anticoagulation or carotid intervention.