Introduction: Lacunar strokes are frequently attributed almost entirely to intrinsic small vessel pathologies like lipohyalinosis and microatherosclerosis, with embolism into small penetrating arteries considered extremely uncommon. By integrating data from neuroimaging and classic neuropathologic studies, this analysis quantifies the contribution of embolism to lacunar ischemic strokes. Methods: Systematic meta-analyses, following PRISMA guidelines, were performed to delineate: (1) the proportion of all ischemic strokes due to lacunar infarcts; (2) the relative frequencies of classic lacunar syndromes including pure motor hemiparesis (PMH), pure sensory stroke (PSS), dysarthria-clumsy hand (DCH), ataxic hemiparesis (AH), and sensorimotor stroke (SMS) among lacunar strokes; and (3) the frequency in neuropathologic serial sectioning studies of embolism (vs lipohyalinosis, microatherosclerosis, intracranial branch origin atherosclerosis, and other) as the causal substrate of each syndromic subtype of lacunar stroke. Results: Across 24 ischemic stroke series totaling 7,700 patients, lacunar strokes comprised 19.5% of ischemic strokes. Among 7 clinical series of 1,646 lacunar stroke patients, syndrome frequencies were: PMH 45.2%, PSS 10.6%, DCH 7.7%, AH 11.2%, SMS 15.7%, and other 8.8%. Among all symptomatic lacunar stroke patients studied neuropathologically with serial sectioning of penetrating arteries, mechanisms were: embolism in 3%, microatherosclerosis in 9.7%, intracranial branch origin atherosclerosis in 2%, and lipohyalinosis in 1.4%. Embolic mechanisms produced PMH, DCH, and AH, but not PSS, lacunar strokes. The embolic sources in these patients were undetermined. Integrating the epidemiologic and neuropathologic data indicated that cardiogenic or arteriogenic emboli are the cause of 20.2% of lacunar ischemic strokes. Conclusion: Embolism into small penetrating arteries is a distinct and important cause of lacunar stroke, accounting for one-fifth of cases, especially syndromes related to larger (PMH, DCH, ACH) than smaller penetrating arteries. Recognizing embolism as a relatively common pathophysiologic mechanism challenges traditional concepts that attribute lacunar strokes mainly to intrinsic small vessel disease. These findings highlight the need for tailored diagnostic and therapeutic strategies addressing embolic sources in small vessel ischemic stroke.
Waghmare et al. (Thu,) studied this question.