Feng Xiao, Tao Wang, Lei Gao, Jian Fang, Zhenmeng Sun, Haibo Xu, Junjian Zhang
Abstract
"Asymptomatic" carotid artery stenosis (aCAS) patients usually have cognitive impairment in the domains of executive, psychomotor speed, and memory function. However, the pathophysiology of this impairment in aCAS patients is still unclear. In this study, amplitude of low-frequency fluctuation (ALFF) method was used based on resting-state blood oxygenation level dependent (BOLD) signals, to investigate local brain activity in 19 aCAS patients and 24 healthy controls, aimed to explore this pathophysiology mechanism. We analyzed this intrinsic activity in four individual frequency bands: Slow-2 (0.198-0.25 Hz), Slow-3 (0.073-0.198 Hz), Slow-4 (0.027-0.073 Hz), and Slow-5 (0.01-0.027 Hz). The aCAS-related ALFF changes were mainly distributed in (1) cortical midline structure, including bilateral dorsomedial prefrontal (dmPFC), cingulate cortex (CC) and precuneus (PCu); (2) hippocampus and its adjacent structures, including bilateral hippocampus, thalamus and medial temporal regions. We found these spatial patterns were frequency-dependent. Significant interaction between frequency and group was found distributed in left putamen, triangle part of inferior temporal and bilateral precentral/postcentral gyrus when Slow-4 and Slow-5 were considered. The delay recall ability of aCAS patient was significantly positive correlated to the mean ALFF in dmPFC within Slow-4 band and the mean ALFF in the bilateral hippocampus within Slow-3 band, respectively. We also found the Montreal Cognitive Assessme score of aCAS patient was significantly positive correlated to the mean ALFF in right fusiform and parahippocampus within Slow-3 band. Furthermore, we built the automatic diagnosis and prediction models based on support vector machine (SVM) and back propagation neural network (BPNN), respectively. Both two types of models could achieve relatively competent performance, which meant the frequency-dependent changes in ALFF could not only reveal the pathophysiology mechanism of cognitive impairment of aCAS, but also could be used as neuroimaging marker in the analysis of cognition impairment for aCAS patients.
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