Mechanisms Involved in Lacunar Infarction and Their Role in Early Neurological Deterioration

Abstract

Background The mechanisms of lacunar infarction are still unclear and may be heterogenous. We aimed to investigate the presence of parent artery atheroma, cerebral vasodilatory function, and blood-brain barrier (BBB) breakdown and their role in the development of early neurological deterioration (END) in patients with acute lacunar infarction. Methods Patients with acute lacunar infarction prospectively underwent transcranial Doppler breath-holding test, contrast-enhanced f luid-attenuated inversion recovery magnetic resonance imaging, and magnetic resonance angiography with/without high-resolution vessel wall imaging to determine the cerebral vasomotor reactivity to carbon dioxide (CO2-CVR) of the symptomatic artery, BBB breakdown, and the presence of branch atheromatous disease in the parent artery, respectively, before the development of END. We compared the presence of each mechanism between patients who developed END and those without END and the role in predicting END between mechanisms. Results Among the 41 patients included, three (7.3%) experienced END. Reduced CO2-CVR, branch atheromatous disease, and widespread BBB breakdown were observed in eight (19.5%), 10 (24.4%), and 11 patients (26.8%), respectively. Among these factors, CO2-CVR was significantly lower in patients with END than in those without END (breath-holding index, 0.64 [interquartile range, 0.47–0.70] vs. 1.05 [0.81–1.33], p=0.028) and best predicted END (area under the curve=0.889; 95% confidence interval, 0.779–0.999; p<0.001). Conclusion Cerebral vasodilatory dysfunction is associated with END in patients with acute lacunar infarction. Our study suggests that CO2-CVR testing has a role in the risk stratification of lacunar infarction, and a confirmatory study is required in the future. Key words: Stroke; Lacunar infarction; Cerebral small vessel diseases; Transcranial Doppler ultrasonography; Blood-brain barrier