本文選題：丘腦梗死 + 軀體感覺(jué)功能障礙　； 參考：《重慶醫(yī)科大學(xué)》2016年博士論文

【摘要】：第一部分慢性丘腦梗死軀體感覺(jué)障礙患者腦結(jié)構(gòu)損害的MRI研究目的:分析慢性丘腦梗死患者丘腦與初級(jí)軀體感覺(jué)皮層(primary somatosensory cortex,S1)之間結(jié)構(gòu)連接和全腦皮層體積改變情況,以及與軀體感覺(jué)功能障礙之間的關(guān)系,旨在探討慢性丘腦梗死患者感覺(jué)功能障礙的神經(jīng)影像機(jī)制。方法:選取31例慢性丘腦梗死患者(梗死組)和31例性別、年齡匹配的正常健康志愿者(對(duì)照組),對(duì)所有受試者的軀體感覺(jué)功能、運(yùn)動(dòng)功能及日常生活能力等方面進(jìn)行評(píng)估,并進(jìn)行MRI全腦高分辨率解剖成像和擴(kuò)散張量成像(diffusion tensor imaging,DTI)掃描。隨后進(jìn)行以下數(shù)據(jù)處理和分析:(1)采用確定性追蹤的方法對(duì)患側(cè)丘腦與S1、健側(cè)丘腦與S1進(jìn)行纖維追蹤,并計(jì)算纖維數(shù)量、各向異性分?jǐn)?shù)(fractional anisotropy,FA)、平均擴(kuò)散系數(shù)(mean diffusivity,MD)、縱向擴(kuò)散率(axial diffusivity,λ‖)和橫向擴(kuò)散率(radial diffusivity,λ⊥)。采用一般線性模型對(duì)兩組的纖維數(shù)量、FA、MD、λ‖和λ⊥值進(jìn)行統(tǒng)計(jì)分析。(2)全腦皮層重建及皮層體積的預(yù)處理采用Freesuefer V5.3軟件,其統(tǒng)計(jì)分析采用一般線性模型比較兩組間的差異,cluster水平FWE校正,P0.05具有統(tǒng)計(jì)學(xué)差異。(3)應(yīng)用中介分析法對(duì)病灶側(cè)丘腦與S1間纖維束的FA值、S1體積和軀體感覺(jué)功能評(píng)分三者之間的關(guān)系進(jìn)行研究。結(jié)果:(1)與對(duì)照組比較,梗死組患側(cè)丘腦與S1間纖維的數(shù)量(F=21.911,P0.001)、FA值(F=18.634,P0.001)顯著低于對(duì)照組,且FA值與軀體感覺(jué)功能有關(guān)(r=0.460,P=0.012);梗死組患側(cè)丘腦-S1纖維束的MD值(F=18.673,P0.001)、λ‖(F=14.356,P0.001)和λ⊥(F=16.985,P0.001)顯著高于對(duì)照組。(2)梗死組健側(cè)丘腦與S1間纖維的數(shù)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)與對(duì)照組無(wú)統(tǒng)計(jì)學(xué)差異。(3)與對(duì)照組比較,梗死組的S1(T=5.401,cluster size=330mm2)、中央溝及M1(T=3.909;,cluster size=247mm2)、緣上回(T=4.002,cluster size=531mm2)體積顯著降低,且S1體積與軀體感覺(jué)功能評(píng)分呈正相關(guān)(r=0.375,P=0.049);(4)梗死組萎縮的S1體積可部分中介患側(cè)丘腦-S1纖維束FA值與軀體感覺(jué)功能之間的關(guān)系,中介效應(yīng)占總效應(yīng)的比例為23.846%。結(jié)論:慢性丘腦梗死患者出現(xiàn)軀體感覺(jué)功能減退可能是由于丘腦與S1間的纖維連接受損及與之相連的S1體積降低所致。第二部分慢性丘腦梗死軀體感覺(jué)障礙患者腦功能連接的靜息態(tài)f MRI研究目的:采用種子點(diǎn)靜息態(tài)功能連接方法及獨(dú)立成分分析(independent component analysis,ICA)方法,分析慢性丘腦梗死患者感覺(jué)運(yùn)動(dòng)網(wǎng)絡(luò)內(nèi)部以及丘腦與全腦靜息態(tài)功能連接的改變,闡明慢性丘腦梗死患者功能連接改變特點(diǎn)及與軀體感覺(jué)障礙的關(guān)系,進(jìn)而揭示軀體感覺(jué)功能恢復(fù)的神經(jīng)機(jī)制。方法:選取31例慢性丘腦梗死患者(梗死組)和31例性別、年齡匹配的正常健康志愿者(對(duì)照組),對(duì)所有受試者的軀體感覺(jué)功能、運(yùn)動(dòng)功能及日常生活能力等方面進(jìn)行評(píng)估,并進(jìn)行MRI全腦高分辨率解剖成像和靜息態(tài)f MRI掃描。隨后進(jìn)行以下數(shù)據(jù)處理和分析:(1)靜息態(tài)f MRI數(shù)據(jù)預(yù)處理采用基于Matlab平臺(tái)的SPM8和DPARSF軟件。(2)ICA采用GIFT軟件,并提取出感覺(jué)運(yùn)動(dòng)網(wǎng)絡(luò)(sensory motor network,SMN)。(3)分別以左側(cè)(或患側(cè))和右側(cè)(或健側(cè))丘腦作為種子點(diǎn)進(jìn)行全腦功能連接分析。(4)比較梗死組和對(duì)照組丘腦與全腦功能連接、感覺(jué)運(yùn)動(dòng)網(wǎng)絡(luò)內(nèi)部功能連接的差異采用一般線性模型,將性別、年齡及全腦體積作為協(xié)變量,單體素閾值取P0.001,多重比較校正采用cluster水平FWE校正。(5)提取出上述組間分析具有統(tǒng)計(jì)學(xué)差異的腦區(qū)作為感興趣區(qū),與軀體感覺(jué)評(píng)分進(jìn)行偏相關(guān)分析,以年齡、性別及全腦體積作為協(xié)變量。結(jié)果:(1)與對(duì)照組比較,梗死組SMN內(nèi)部功能連接顯著增強(qiáng)的腦區(qū)有:患側(cè)輔助運(yùn)動(dòng)區(qū)(T=4.658,體素=46);功能連接減弱的腦區(qū)有:患側(cè)中央后回和頂上小葉(T=4.581,體素=171)。(2)梗死組患側(cè)輔助運(yùn)動(dòng)區(qū)功能連接值與軀體感覺(jué)功能評(píng)分呈正相關(guān)(r=0.426,P=0.027)。(3)以左側(cè)(患側(cè))丘腦為種子點(diǎn),梗死組在下列腦區(qū)功能連接較對(duì)照組增強(qiáng):患側(cè)初級(jí)感覺(jué)皮層和初級(jí)運(yùn)動(dòng)皮層(T=4.479,體素=273)、健側(cè)初級(jí)感覺(jué)皮層和初級(jí)運(yùn)動(dòng)皮層(T=4.386,體素=1131)、枕中回和枕下回(T=4.832,體素=787)。(4)以右側(cè)(健側(cè))丘腦為種子點(diǎn),梗死組在下列腦區(qū)功能連接較對(duì)照組增強(qiáng):患側(cè)初級(jí)感覺(jué)皮層和初級(jí)運(yùn)動(dòng)皮層(T=4.108,體素=708)、健側(cè)初級(jí)感覺(jué)皮層和初級(jí)運(yùn)動(dòng)皮層(T=5.177,體素=2947)、健側(cè)顳中回(T=5.213,體素=614)。(5)患側(cè)丘腦與患側(cè)初級(jí)感覺(jué)運(yùn)動(dòng)皮層功能連接值與軀體感覺(jué)功能評(píng)分呈正相關(guān)(r=0.371,P=0.048);健側(cè)丘腦與患側(cè)初級(jí)感覺(jué)運(yùn)動(dòng)皮層功能連接值與軀體感覺(jué)功能評(píng)分呈正相關(guān)(r=0.396,P=0.041)。結(jié)論:慢性丘腦梗死患者軀體感覺(jué)功能減退可能與SMN內(nèi)部患側(cè)S1區(qū)功能連接減弱有關(guān),而其患側(cè)輔助運(yùn)動(dòng)區(qū)功能連接增加,可能反映了功能的重構(gòu)。此外,患者雙側(cè)S1與丘腦功能連接增強(qiáng)可能也發(fā)揮了功能代償作用。第三部分慢性丘腦梗死患者初級(jí)感覺(jué)皮層結(jié)構(gòu)損害與功能重構(gòu)的關(guān)系目的:分析慢性丘腦梗死患者患側(cè)丘腦-初級(jí)感覺(jué)皮層(primary sensory cortex,S1)結(jié)構(gòu)連接、S1-S1結(jié)構(gòu)連接、患側(cè)丘腦-S1功能連接、S1-S1功能連接改變,以及它們之間的相互關(guān)系。旨在進(jìn)一步探討慢性丘腦梗死患者軀體感覺(jué)障礙發(fā)生的原因和功能重構(gòu)的方式,以及結(jié)構(gòu)連接損害和功能重構(gòu)的關(guān)系。方法:選取31例慢性丘腦梗死患者(梗死組)和31例性別、年齡匹配的正常健康志愿者(對(duì)照組),對(duì)所有被試的軀體感覺(jué)功能、運(yùn)動(dòng)功能及日常生活能力等方面進(jìn)行評(píng)估,并進(jìn)行MRI全腦高分辨率解剖成像、DTI和靜息態(tài)f MRI掃描。隨后進(jìn)行以下數(shù)據(jù)處理和分析:(1)DTI數(shù)據(jù)預(yù)處理采用基于Linux平臺(tái)的FSL 5.1軟件包;靜息態(tài)f MRI數(shù)據(jù)預(yù)處理采用基于Matlab平臺(tái)的SPM8和DPARSF軟件。(2)采用確定性追蹤的方法對(duì)患側(cè)丘腦與S1區(qū),雙側(cè)S1區(qū)進(jìn)行纖維追蹤,并計(jì)算各纖維束的FA值。兩組纖維束的FA值比較采用一般線性模型進(jìn)行統(tǒng)計(jì)分析,將性別、年齡和全腦體積作為協(xié)變量。(3)患側(cè)丘腦-S1、S1-S1功能連接采用REST軟件進(jìn)行計(jì)算,并提取出所有受試者的功能連接值。采用一般線性模型比較兩組患側(cè)丘腦-S1、S1-S1功能連接值的差異,性別、年齡及全腦體積作為協(xié)變量。(4)梗死組分別做下列偏相關(guān)分析:患側(cè)丘腦-S1纖維束FA值與S1-S1纖維束FA值、患側(cè)丘腦-S1纖維束FA值與患側(cè)丘腦-S1功能連接值、患側(cè)丘腦-S1纖維束FA值與S1-S1功能連接值、S1-S1纖維束FA值與S1-S1功能連接值之間。結(jié)果:(1)梗死組患側(cè)丘腦-S1纖維束(F=18.634,P0.001)、S1-S1纖維束(F=36.226,P0.001)FA值較對(duì)照組顯著降低。(2)梗死組患側(cè)丘腦-S1功能連接值(F=7.888,P=0.007)、S1-S1功能連接值(F=23.930,P0.001)顯著高于對(duì)照組。(3)梗死組患側(cè)丘腦-S1纖維束FA值與S1-S1纖維束FA值呈正相關(guān)(r=0.466,P=0.012);患側(cè)丘腦-S1纖維束FA值與S1-S1功能連接值呈負(fù)相關(guān)(r=-0.388,P=0.041);S1-S1纖維束FA值與S1-S1功能連接值呈負(fù)相關(guān)(r=-0.554,P=0.002)。結(jié)論:慢性丘腦梗死患者出現(xiàn)軀體感覺(jué)障礙可能與患側(cè)丘腦-S1結(jié)構(gòu)連接受損以及繼發(fā)性的S1-S1結(jié)構(gòu)連接損傷有關(guān);S1-S1功能連接增強(qiáng)可能為彌補(bǔ)這些結(jié)構(gòu)連接受損的一種代償方式。
[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.

【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類號(hào)】：R743.33;R445.2

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