Patients with subcortical ischemic vascular disease (SIVD) exhibit a high risk of cognitive impairment that might be caused by neurologic deficits and vascular injuries. However, the mechanism remains unknown. In current study, 24 normal controls (NC) and 54 SIVD patients, including 26 SIVD patients with no cognitive impairment (SIVD-NCI) and 28 SIVD patients with mild cognitive impairment (SIVD-MCI) underwent the resting-state functional MRI (rs-fMRI) and neuropsychological assessments. We combined regional homogeneity (ReHo) and cerebral blood flow (CBF) by using the global ReHo-CBF correlations coefficient and the ReHo/CBF ratio to detect the inner link between neuronal activity and vascular responses. Correlations between the ReHo/CBF ratio and neuropsychological assessments were explored in patients with SIVD. As a result, we identified significantly decreased global ReHo-CBF coupling in the SIVD-NCI group and SIVD- MCI group with respect to the NC. The SIVD-MCI group showed more serious decoupling of the global ReHo-CBF correlation. We also found a significantly abnormal ReHo/CBF ratio predominantly located in cognitive-related brain regions, including the left insula, right middle temporal gyrus, right precuneus, left precentral gyrus, and left inferior parietal lobule but not the supramarginal and angular gyri. The SIVD-MCI group showed more severe disorders of neurovascular coupling than the other two groups. Moreover, the ReHo/CBF ratio in the left precentral gyrus of the SIVD-NCI group exhibited a positive correlation with the MMSE scores. These findings suggested that patients with SIVD show abnormal neurovascular coupling at the early stage of the disease and during disease development. It might be associated with disease severity and cognitive impairment. Neurovascular decoupling in brain may be a possible neuropathological mechanism of SIVD.
Subcortical ischemic vascular disease (SIVD) is a major cause of vascular cognitive impairment (CI) and features extensive atrophy in the cerebral cortex. We aimed to test the hypothesis that cognitive deficits in SIVD are linked to decreased cortical thickness in specific brain regions, which may constitute neuroimaging biomarkers of CI. Sixty-seven SIVD patients without (SIVD-NC, n = 35) and with (SIVD-CI, n = 32) CI and a group of healthy controls (HCs, n = 36) underwent structural magnetic resonance imaging (MRI) and cognitive functional assessments. FreeSurfer was used to preprocess structural MRI data and to calculate and compare cortical thickness. The correlation between cortical thickness and cognitive scores was examined in SIVD patients. Significantly altered cortical thickness in the bilateral insula, middle and inferior temporal lobes, precuneus, and medial temporal lobe (MTL) was identified among the three groups (p < 0.05, Monte Carlo simulation corrected). Post hoc results showed significantly decreased thickness in the bilateral insula and temporal lobe in SIVD-NC and SIVD-CI patients compared with HCs. However, the areas with reduced cortical thickness were larger in SIVD-CI than SIVD-NC patients. SIVD-CI patients had significantly reduced thickness in the bilateral precuneus and left MTL (Bonferroni corrected) compared with SIVD-NC patients when we extracted the mean thickness for each region of interest. In SIVD patients, the thicknesses of the left MTL and bilateral precuneus were positively correlated with immediate recall in the memory test. SIVD might lead to extensive cerebral cortical atrophy, while atrophy in the MTL and precuneus might be associated with memory deficits.
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