Abstract

Lacunar stroke has been a recognized stroke subtype for many years but its pathophysiology remains unknown, so prevention and treatment are suboptimal. Most lacunar strokes result from an intrinsic cerebral small vessel disease, probably part of a systemic disorder. Hypertension, diabetes and other vascular risk factors (but not atrial fibrillation and ipsilateral carotid stenosis) are equally common in lacunar as in large artery atherothromboembolic stroke, which, together with other factors, suggests that the patient’s response to vascular risk factors, not the vascular risk factors per se, determines whether they develop small vessel or large artery stroke. Inflammation and endothelial failure are probably involved in the pathogenesis of lacunar stroke, but their role needs to be clarified. The cerebral venules as well as arterioles are abnormal in this condition. The disorder may not be primarily ischemic; instead, arteriolar thrombosis may be a late-stage phenomenon secondary to chronic arteriolar wall damage resulting from leakage of plasma components across the BBB. Accurate diagnosis of lacunar stroke, avoiding risk factor-based classifications, is required to underpin future research.

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