静息态功能磁共振成像观察阿尔茨海默病患者大脑自发活动特点

Spontaneous activities in Alzheimer＇ s disease explored by resting state functional magnetic resonance imaging

目的运用静息态功能磁共振成像（fMRI）技术探测老年阿尔茨海默病（AD）患者大脑自发活动特点。方法选择23例AD患者（AD组）和21名健康志愿者（NC组），分别接受神经心理学检查（MMSE、听觉词语学习测试）和静息态fMRI扫描，比较两组间神经心理评分和局部一致性（ReHo）的差异。结果AD组（分）MMSE（20±4）、听觉词语学习测试即刻回忆（2．6±1．6）、延迟回忆（0．4±0．7）及再认成绩（5．8±3．7）均低于NC组（29±1、5．9±1．2、5．5±2．0、9．2±1．1，T=10．58、7．21、10．99、3．96，均P〈0．01）；当设置单个体素统计阈值为P〈0．01、激活簇≥100体素时，与NC组比较，AD组在前额叶内侧面、后扣带回及楔前叶、右侧颞上回、两侧顶上小叶及顶下小叶等默认网络脑区ReHo值降低；在左侧壳核、丘脑的ReHo值增高。结论AD患者存在大脑默认功能网络异常；而在壳核、丘脑的自发活动增强，可能是大脑皮质下结构对默认系统功能降低的代偿反应。

Objective To investigate the characteristics of spontaneous activities throughout the whole brain with Alzheimer＇ s disease （AD） by resting state functional magnetic resonance imaging （fMRI）. Methods The subjects included 23 AD patients and 21 normal controls （NC）, who underwent a neuropsychological test battery including MMSE and Auditory Verbal Learning Test （AVLT） and resting- state fMRI using GE Signa 3.0 T MR scanner. The neuropsychologieal scores were compared between two groups. Regional homogeneity （ReHo） method was used to explore the different regional spontaneous activities throughout the brain between normal controls and patients with AD. Results In AD group, clinical variables （ MMSE scores ： 20 ± 4, AVLT-Immediate Recall ： 2. 6 ± 1.6, AVLT-DeIay Recall ： 0. 4 ± 0. 7, AVLT-Recognition： 5.8 ±3.7） were lower than NC group（29 ± 1,5.9 ± 1.2, 5.5 ±2. 0, 9. 2 ± 1.1, T = 10. 58,7.21,10. 99,3.96, all P 〈 0. 01 ）. With the threshold of P 〈 0. 01 for each voxel and a cluster size of at least 100 voxels, decreased ReHo indexes were found in default mode network （DMN） including the medial prefrontal cortex, posterior cingulate gyrus/precuneus, right superior temporal gyrus and bilateral superior parietal lobule/inferior parietal lobule in AD, while increased ReHo indexes were found in left putamen and thalamus compared with controls. Conclusion The DMN are damaged in AD and spontaneous activities of putamen and thalamus are reinforced as compensation response of subcortical structures.