Structural changes in white matter lesion patients and their correlation with cognitive impairment

白质病变患者的结构变化及其与认知障碍的相关性

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Abstract

BACKGROUND: White matter lesions (WMLs) play a role in cognitive decline and dementia. Little is known about gray matter (GM) changes in WMLs. This study aimed to investigate GM changes in WML patients. MATERIALS AND METHODS: Correlations between altered structural volume and cognitive assessment scores were investigated. GM and white matter (WM) changes in 23 WML-vascular dementia (VaD) patients, 22 WML-non-dementia vascular cognitive impairment (VCIND) patients, and 23 healthy control (HC) subjects were examined. Gray matter density (GMD) was calculated by measuring local proportions of GM at thousands of homologous cortical locations. WM volume was obtained by fully automated software using voxel-based morphometry (VBM). RESULTS: Widespread GMD was significantly lower in WML patients compared to control subjects in cortical and subcortical regions (p<0.05). Greatest differences were found in the bilateral anterior cingulate cortex, inferior frontal gyrus, insula, angular gyrus, caudate, precentral gyrus, and right middle temporal gyrus, right thalamus. Secondary region of interest (ROI) analysis indicated significantly greater GMD in the bilateral caudate among WML-VCIND patients (n=22) compared to HCs (p<0.05). There was a significant difference in WM volume between WML patients and control subjects (p<0.05). Greatest differences were located in the genu/body/splenium of the corpus callosum and superior corona radiata L, and posterior corona radiata L. There was a significant association between structural changes and cognitive scores (Montreal Cognitive Assessment [MoCA] score) (p<0.05). There was no significant correlation between structural changes and Mini Mental State Examination (MMSE) scores (p>0.05). CONCLUSION: GMD and WM volume were changed in WMLs, and the changes were detectable. Correlation between structural changes and cognitive function was promising in understanding the pathological and physiological mechanisms of WMLs.

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