慢性丘脑梗死躯体感觉障碍患者脑结构损害和功能重构的MRI研究

发布时间：2018-05-13 07:46

本文选题：丘脑梗死 + 躯体感觉功能障碍　；参考：《重庆医科大学》2016年博士论文

【摘要】：第一部分慢性丘脑梗死躯体感觉障碍患者脑结构损害的MRI研究目的:分析慢性丘脑梗死患者丘脑与初级躯体感觉皮层(primary somatosensory cortex,S1)之间结构连接和全脑皮层体积改变情况,以及与躯体感觉功能障碍之间的关系,旨在探讨慢性丘脑梗死患者感觉功能障碍的神经影像机制。方法:选取31例慢性丘脑梗死患者(梗死组)和31例性别、年龄匹配的正常健康志愿者(对照组),对所有受试者的躯体感觉功能、运动功能及日常生活能力等方面进行评估,并进行MRI全脑高分辨率解剖成像和扩散张量成像(diffusion tensor imaging,DTI)扫描。随后进行以下数据处理和分析:(1)采用确定性追踪的方法对患侧丘脑与S1、健侧丘脑与S1进行纤维追踪,并计算纤维数量、各向异性分数(fractional anisotropy,FA)、平均扩散系数(mean diffusivity,MD)、纵向扩散率(axial diffusivity,λ‖)和横向扩散率(radial diffusivity,λ⊥)。采用一般线性模型对两组的纤维数量、FA、MD、λ‖和λ⊥值进行统计分析。(2)全脑皮层重建及皮层体积的预处理采用Freesuefer V5.3软件,其统计分析采用一般线性模型比较两组间的差异,cluster水平FWE校正,P0.05具有统计学差异。(3)应用中介分析法对病灶侧丘脑与S1间纤维束的FA值、S1体积和躯体感觉功能评分三者之间的关系进行研究。结果:(1)与对照组比较,梗死组患侧丘脑与S1间纤维的数量(F=21.911,P0.001)、FA值(F=18.634,P0.001)显著低于对照组,且FA值与躯体感觉功能有关(r=0.460,P=0.012);梗死组患侧丘脑-S1纤维束的MD值(F=18.673,P0.001)、λ‖(F=14.356,P0.001)和λ⊥(F=16.985,P0.001)显著高于对照组。(2)梗死组健侧丘脑与S1间纤维的数量(F=0.062,P=0.804)、FA值(F=0.079,P=0.779)、MD值(F=0.100,P=0.753)、λ‖(F=0.227,P=0.636)和λ⊥(F=0.432,P=0.513)与对照组无统计学差异。(3)与对照组比较,梗死组的S1(T=5.401,cluster size=330mm2)、中央沟及M1(T=3.909;,cluster size=247mm2)、缘上回(T=4.002,cluster size=531mm2)体积显著降低,且S1体积与躯体感觉功能评分呈正相关(r=0.375,P=0.049);(4)梗死组萎缩的S1体积可部分中介患侧丘脑-S1纤维束FA值与躯体感觉功能之间的关系,中介效应占总效应的比例为23.846%。结论:慢性丘脑梗死患者出现躯体感觉功能减退可能是由于丘脑与S1间的纤维连接受损及与之相连的S1体积降低所致。第二部分慢性丘脑梗死躯体感觉障碍患者脑功能连接的静息态f MRI研究目的:采用种子点静息态功能连接方法及独立成分分析(independent component analysis,ICA)方法,分析慢性丘脑梗死患者感觉运动网络内部以及丘脑与全脑静息态功能连接的改变,阐明慢性丘脑梗死患者功能连接改变特点及与躯体感觉障碍的关系,进而揭示躯体感觉功能恢复的神经机制。方法:选取31例慢性丘脑梗死患者(梗死组)和31例性别、年龄匹配的正常健康志愿者(对照组),对所有受试者的躯体感觉功能、运动功能及日常生活能力等方面进行评估,并进行MRI全脑高分辨率解剖成像和静息态f MRI扫描。随后进行以下数据处理和分析:(1)静息态f MRI数据预处理采用基于Matlab平台的SPM8和DPARSF软件。(2)ICA采用GIFT软件,并提取出感觉运动网络(sensory motor network,SMN)。(3)分别以左侧(或患侧)和右侧(或健侧)丘脑作为种子点进行全脑功能连接分析。(4)比较梗死组和对照组丘脑与全脑功能连接、感觉运动网络内部功能连接的差异采用一般线性模型,将性别、年龄及全脑体积作为协变量,单体素阈值取P0.001,多重比较校正采用cluster水平FWE校正。(5)提取出上述组间分析具有统计学差异的脑区作为感兴趣区,与躯体感觉评分进行偏相关分析,以年龄、性别及全脑体积作为协变量。结果:(1)与对照组比较,梗死组SMN内部功能连接显著增强的脑区有:患侧辅助运动区(T=4.658,体素=46);功能连接减弱的脑区有:患侧中央后回和顶上小叶(T=4.581,体素=171)。(2)梗死组患侧辅助运动区功能连接值与躯体感觉功能评分呈正相关(r=0.426,P=0.027)。(3)以左侧(患侧)丘脑为种子点,梗死组在下列脑区功能连接较对照组增强:患侧初级感觉皮层和初级运动皮层(T=4.479,体素=273)、健侧初级感觉皮层和初级运动皮层(T=4.386,体素=1131)、枕中回和枕下回(T=4.832,体素=787)。(4)以右侧(健侧)丘脑为种子点,梗死组在下列脑区功能连接较对照组增强:患侧初级感觉皮层和初级运动皮层(T=4.108,体素=708)、健侧初级感觉皮层和初级运动皮层(T=5.177,体素=2947)、健侧颞中回(T=5.213,体素=614)。(5)患侧丘脑与患侧初级感觉运动皮层功能连接值与躯体感觉功能评分呈正相关(r=0.371,P=0.048);健侧丘脑与患侧初级感觉运动皮层功能连接值与躯体感觉功能评分呈正相关(r=0.396,P=0.041)。结论:慢性丘脑梗死患者躯体感觉功能减退可能与SMN内部患侧S1区功能连接减弱有关,而其患侧辅助运动区功能连接增加,可能反映了功能的重构。此外,患者双侧S1与丘脑功能连接增强可能也发挥了功能代偿作用。第三部分慢性丘脑梗死患者初级感觉皮层结构损害与功能重构的关系目的:分析慢性丘脑梗死患者患侧丘脑-初级感觉皮层(primary sensory cortex,S1)结构连接、S1-S1结构连接、患侧丘脑-S1功能连接、S1-S1功能连接改变,以及它们之间的相互关系。旨在进一步探讨慢性丘脑梗死患者躯体感觉障碍发生的原因和功能重构的方式,以及结构连接损害和功能重构的关系。方法:选取31例慢性丘脑梗死患者(梗死组)和31例性别、年龄匹配的正常健康志愿者(对照组),对所有被试的躯体感觉功能、运动功能及日常生活能力等方面进行评估,并进行MRI全脑高分辨率解剖成像、DTI和静息态f MRI扫描。随后进行以下数据处理和分析:(1)DTI数据预处理采用基于Linux平台的FSL 5.1软件包;静息态f MRI数据预处理采用基于Matlab平台的SPM8和DPARSF软件。(2)采用确定性追踪的方法对患侧丘脑与S1区,双侧S1区进行纤维追踪,并计算各纤维束的FA值。两组纤维束的FA值比较采用一般线性模型进行统计分析,将性别、年龄和全脑体积作为协变量。(3)患侧丘脑-S1、S1-S1功能连接采用REST软件进行计算,并提取出所有受试者的功能连接值。采用一般线性模型比较两组患侧丘脑-S1、S1-S1功能连接值的差异,性别、年龄及全脑体积作为协变量。(4)梗死组分别做下列偏相关分析:患侧丘脑-S1纤维束FA值与S1-S1纤维束FA值、患侧丘脑-S1纤维束FA值与患侧丘脑-S1功能连接值、患侧丘脑-S1纤维束FA值与S1-S1功能连接值、S1-S1纤维束FA值与S1-S1功能连接值之间。结果:(1)梗死组患侧丘脑-S1纤维束(F=18.634,P0.001)、S1-S1纤维束(F=36.226,P0.001)FA值较对照组显著降低。(2)梗死组患侧丘脑-S1功能连接值(F=7.888,P=0.007)、S1-S1功能连接值(F=23.930,P0.001)显著高于对照组。(3)梗死组患侧丘脑-S1纤维束FA值与S1-S1纤维束FA值呈正相关(r=0.466,P=0.012);患侧丘脑-S1纤维束FA值与S1-S1功能连接值呈负相关(r=-0.388,P=0.041);S1-S1纤维束FA值与S1-S1功能连接值呈负相关(r=-0.554,P=0.002)。结论:慢性丘脑梗死患者出现躯体感觉障碍可能与患侧丘脑-S1结构连接受损以及继发性的S1-S1结构连接损伤有关;S1-S1功能连接增强可能为弥补这些结构连接受损的一种代偿方式。
[Abstract]:Part one MRI study of brain structural damage in patients with somatosensory disorders in chronic thalamus infarction: to analyze the structural connections between the thalamus and the primary somatosensory cortex (primary somatosensory cortex (S1)) and the changes in the volume of the total cerebral cortex, and the relationship between the somatosensory dysfunction and the somatosensory dysfunction in the patients with chronic thalamic infarction. The neuroimaging mechanism of sensory dysfunction in patients with chronic thalamus infarction. Methods: 31 patients with chronic thalamus infarction (infarct group) and 31 sex, age matched normal healthy volunteers (control group) were used to evaluate the somatosensory function, motor function and daily living ability of all subjects, and the high score of MRI whole brain was carried out. The following data processing and analysis were followed: (1) fiber tracking was performed on the affected thalamus and S1, the healthy side thalamus and S1 by deterministic tracking, and the number of fibers, the isotropic fraction (fractional anisotropy, FA) and the average diffusion coefficient (mean DI) were calculated. (1) the method of deterministic tracking was used to track the affected thalamus and S1, the healthy side of the thalamus and S1. Ffusivity, MD), longitudinal diffusivity (axial diffusivity, lambda) and transverse diffusion rate (radial diffusivity, lambda). A general linear model is used to analyze the number of two groups of fibers, FA, MD, lambda and lambda values. (2) complete cerebral cortex reconstruction and cortical volume preprocessing using Freesuefer V5.3 software, and its statistical analysis uses general linearity. The model was compared between the two groups, cluster level FWE correction and P0.05 had statistical difference. (3) the relationship between the FA value of the lateral thalamus and S1 fiber bundles, the volume of S1 and the somatosensory function score between the three groups were studied. Results: (1) the number of the thalamus and S1 fibers in the infarction group (F=21.91) was compared with the control group (F=21.91). 1, P0.001), the value of FA (F=18.634, P0.001) was significantly lower than that of the control group, and the FA value was related to the somatosensory function (r=0.460, P=0.012), and the MD value of the -S1 fiber bundle in the lateral thalamus (F=18.673, P0.001) in the infarction group was significantly higher than that of the control group. (2) the number of the fibers in the healthy lateral thalamus of the infarct group. FA value (F=0.079, P=0.779), MD value (F=0.100, P=0.753), lambda (F=0.227, P=0.636) and lambda (F=0.432, P=0.513) have no statistical difference from the control group. (3) compared with the control group, the S1 (T=5.401, MD) in the infarct group and the upper margin of the upper margin were significantly reduced. There was a positive correlation between volume and somatosensory function score (r=0.375, P=0.049); (4) the S1 volume of atrophy in the infarct group could partly mediate the relationship between the FA value of the -S1 fiber bundle of the thalamus and the somatosensory function. The proportion of the mediator effect to the total effect was 23.846%. conclusion: the hypothalamus may be caused by the hypothalamus due to the hypothalamus in the patients with chronic cerebral infarction. Impairment of fibrous connection with S1 and the decrease of S1 volume associated with it. Second part of the resting state f MRI study of brain functional connections in patients with chronic thalamic infarct: Objective To analyze chronic thalamic infarction by means of resting state function connection and independent component analysis (independent component analysis, ICA). The changes in the interior of the sensory motor network and the resting state function of the thalamus and the whole brain were changed to clarify the characteristics of the functional connection and the relationship with the somatosensory disorder in the patients with chronic thalamus infarction, and then to reveal the neural mechanism of the recovery of somatosensory function. Methods: 31 patients with chronic cerebral infarction (infarct group) and 31 cases of sex and age were selected. The normal healthy volunteers (control group) were used to evaluate the somatosensory function, exercise function and daily living ability of all the subjects, and carry out the MRI whole brain high-resolution imaging and resting state f MRI scan. The following data were processed and analyzed: (1) the resting state f MRI data preprocessing was based on the Matlab platform SPM8 and DPARSF software. (2) ICA uses the GIFT software and extracts the sensory movement network (sensory motor network, SMN). (3) the whole brain function connection analysis is performed on the left (or the affected side) and the right (or the healthy side) thalamus respectively. (4) compare the infarct group and the group of the hypothalamus and the whole brain, and the functional connection inside the sensory motion network. The difference was based on the general linear model, taking the gender, age and whole brain volume as the covariate, the threshold of the monosomal element was P0.001, and the multiple comparison was corrected by the cluster level FWE correction. (5) the brain regions with statistical differences between the above groups were extracted as the region of interest, and the partial correlation analysis was carried out with the somatosensory score, with age, sex and whole brain. Volume as a covariate. Results: (1) compared with the control group, the cerebral area of the SMN internal functional connection in the infarction group was significantly enhanced by the affected side of the affected side (T=4.658, voxel =46); the functional connection weakened in the brain area: the central posterior central gyrus and the superior lobule (T=4.581, voxel =171). (2) the function connection value and the somatosensory work of the affected side motor area of the infarction group The score was positively correlated (r=0.426, P=0.027). (3) the hypothalamus was seeded on the left side (the affected side), and the infarct group was enhanced in the following brain areas than the control group: the primary sensory cortex and the primary motor cortex (T=4.479, voxel =273), the contralateral primary sensory cortex and the primary motor cortex (T=4.386, voxel =1131), the middle occipital and the lower occipital gyrus (T=4.832, body). (4) (4) the hypothalamus was seeded on the right side (the healthy side), and the infarct group was enhanced in the following brain areas than the control group: the primary sensory cortex and the primary motor cortex (T=4.108, voxel =708), the contralateral primary sensory cortex and the primary motor cortex (T=5.177, voxel =2947), the contralateral middle temporal gyrus (T=5.213, voxel =614). (5) the lateral thalamus and the initial side of the affected side. The functional connection value of the sensorimotor cortex was positively correlated with the somatosensory function score (r=0.371, P=0.048); the functional connection value of the healthy side thalamus and the primary sensory motor cortex was positively correlated with the somatosensory function score (r=0.396, P=0.041). Conclusion: the somatosensory function of the patients with chronic thalamic infarction may be associated with the side S1 area work within the SMN. In addition, the functional reconfiguration of bilateral S1 and thalamus may also play a functional compensatory role. The relationship between structural damage and functional remodeling in the primary sensory cortex of third patients with chronic thalamus infarction is to analyze the chronic thalamus. The structural connection of the thalamus primary sensory cortex (primary sensory cortex, S1), the S1-S1 structure connection, the -S1 function connection in the thalamus, the S1-S1 function connection, and the relationship between them, and the relationship between them, are designed to further explore the causes of the somatosensory disorder and the way of functional remodeling in the patients with chronic thalamus infarction, as well as the knot. Methods: 31 cases of chronic thalamus infarction (infarct group) and 31 sex, age matched normal healthy volunteers (control group) were selected to evaluate all the subjects' somatosensory function, exercise function and daily living ability, and MRI high resolution imaging of whole brain, DTI and The resting state f MRI scan. Followed by the following data processing and analysis: (1) DTI data preprocessing using Linux platform based FSL 5.1 software package; resting f MRI data preprocessing using SPM8 and DPARSF software based on Matlab platform. (2) using deterministic tracking method for the affected side thalamus and S1 region, bilateral S1 region fiber tracking, and calculation. The FA value of the fiber bundles. The FA value of the two groups of fiber bundles was compared with the general linear model, and the sex, age and whole brain volume were used as the covariate. (3) the -S1 of the thalamus, the S1-S1 functional connection was calculated by REST software, and the functional connection values of all the subjects were extracted. The two groups of the lateral thalamus were compared with the general linear model. -S1, S1-S1 function connection values, sex, age and total brain volume as covariate. (4) the infarct group did the following partial correlation analysis: the FA value of the -S1 fiber bundle in the thalamus and the FA value of the S1-S1 fiber bundle, the FA value of the -S1 fiber bundle in the thalamus and the -S1 function of the thalamus, the FA value of the -S1 fiber bundle of the thalamus and the connection value of the S1-S1 function. The results were as follows: (1) the -S1 fiber bundle (F=18.634, P0.001) of the thalamus and the FA value of S1-S1 fiber bundle (F=36.226, P0.001) in the infarction group were significantly lower than that of the control group. (2) the -S1 function connection value of the thalamus in the infarction group (F=7.888, P=0.007) was significantly higher than that of the control group. (3) the infarction group suffered from the infarction group. (3) the infarction group suffered from the infarction group. (3) the infarction group suffered from the infarction group. The FA value of the -S1 fiber bundle in the lateral thalamus was positively correlated with the FA value of S1-S1 fiber bundle (r=0.466, P=0.012); the FA value of the -S1 fiber bundle in the thalamus was negatively correlated with the S1-S1 function connection value (r=-0.388, P=0.041). The -S1 structural connections in the thalamus and secondary S1-S1 structural connections are associated with damage, and the enhancement of S1-S1 function connection may be a compensatory way to compensate for the impairment of these structural connections.

【学位授予单位】：重庆医科大学
【学位级别】：博士
【学位授予年份】：2016
【分类号】：R743.33;R445.2

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