论文部分内容阅读
目的探讨躯体形式障碍脑静息态低频振幅(amplitude of low frequency fluctuation,ALFF)改变特点。方法纳入21例躯体形式障碍(somatoform disorders,SFD)患者和21例年龄、性别、受教育水平严格匹配的正常对照(normal control,NC),使用3.0T磁共振扫描仪采集T2WI、T1WI结构像及静息态功能像数据。对两组受试者的ALFF map行组内和组间比较,并采用Alpha Sim(P<0.01,体素数>40)进行多重比较校正。然后提取差异脑区的ALFF值与临床数据进行相关性分析。结果与NC组比较,SFD组ALFF值增高的脑区有:双侧前额叶、双侧前扣带回;ALFF值减低的脑区有:右侧颞叶颞中回、左侧岛叶、左侧旁中央小叶双侧中央后回。SFD组蒙特利尔认知评估量表(Mo CA量表)评分与左侧腹内侧前额叶ALFF值呈显著负相关(r=-0.564,P=0.008),症状自评量表(SCL-90)评分与左侧岛叶ALFF值呈显著负相关(r=-0.505,P=0.020),病程与右侧颞叶ALFF值呈显著负相关(r=-0.514,P=0.017)。结论 SFD患者脑静息态神经元自发活动存在广泛改变,这些异常活动可部分阐释躯体形式障碍的神经生理基础。
Objective To investigate the changes of resting amplitude of low frequency fluctuation (ALFF) in somatization disorders. Methods Twenty-one patients with somatoform disorders (SFD) and 21 normal controls (NCs) with strict age, sex and education level were enrolled in the study. T2WI and T1WI structures were collected using a 3.0T magnetic resonance scanner Resting state functions like data. Intra-and inter-group comparisons were performed on the ALFF map of both groups and multiple comparisons were performed using Alpha Sim (P <0.01, number of voxels> 40). Then extract the ALFF value of different brain regions and clinical data correlation analysis. Results Compared with NC group, the brain areas with increased ALFF value in SFD group were: bilateral prefrontal cortex and bilateral anterior cingulate gyrus; the areas with reduced ALFF value included right temporal lobe, middle left lobe, Lateral central leaflets bilateral central back. The Montreal Cognitive Assessment Scale (Mo CA Scale) score was significantly negatively correlated with the left ventricular prefrontal ALFF score in the SFD group (r = -0.564, P = 0.008), the Symptom Checklist of Symptoms Scale (SCL-90) (R = -0.505, P = 0.020). There was a significant negative correlation between the course of disease and ALFF in the right temporal lobe (r = -0.514, P = 0.017). Conclusion The spontaneous activity of resting resting neurons in patients with SFD varies widely. These abnormal activities may partially explain the neurophysiological basis of somatoform disorders.