腦白質(zhì)高信號的磁共振影像學研究
本文關鍵詞: 腦白質(zhì)高信號 磁敏感加權成像 體素內(nèi)不相干運動 彌散張量成像 深髓靜脈 灌注 認知改變 出處:《浙江大學》2017年博士論文 論文類型:學位論文
【摘要】:腦白質(zhì)高信號(white matter hyperintensities,WMH)是表現(xiàn)為在磁共振T2加權像或T2液體衰減反轉(zhuǎn)恢復序列上,雙側(cè)側(cè)腦室周圍或皮質(zhì)下白質(zhì)多發(fā)的點狀、斑片狀或融合性高信號。有研究表明90%以上的老年人存在WMH。WMH過去被認為是一種與年齡相關的正常生理改變,但近年的研究表明,WMH是卒中、癡呆、抑郁等疾病發(fā)生的高危風險因素,研究WMH的發(fā)生發(fā)展機制及其與腦功能結(jié)構(gòu)異常、行為功能損害的關系具有重要臨床價值。本研究主要基于多模態(tài)磁共振成像(MRI)技術,采用磁敏感加權成像、彌散張量成像、體素內(nèi)不相干運動等方法,探索WMH的發(fā)生機制、以及WMH在認知功能下降中的作用機制。主要內(nèi)容包括以下三部分:第一部分腦白質(zhì)高信號發(fā)生的靜脈源性機制研究研究顯示大腦靜脈膠原纖維化所致靜脈回流障礙與WMH有關,但缺乏客觀的在體研究證據(jù)。我們通過磁共振磁敏感成像技術量化腦深髓靜脈擴張或缺血與WMH嚴重程度的相關性。本研究回顧分析了 158例WMH患者和50例對照組患者的臨床和檢驗數(shù)據(jù),在3TMRI上以磁敏感加權成像方法測量了深髓靜脈體素數(shù)量和用T2 Flair測量WMH組織體積(作為WMH嚴重度的指標)。隨后,對體素數(shù)量和WMH體積的相關性進行線性回歸分析和Pearson相關性分析。WMH患者的深髓靜脈體素數(shù)量明顯高于對照組。增加的深髓靜脈體素數(shù)量同時與全腦WMH體積和對年齡和病灶數(shù)量因素調(diào)整后的局部的WMH體積獨立相關。本研究顯示腦深部靜脈血流不足或缺血在WMH的發(fā)病機理中發(fā)揮重要作用,作為WMH患者的預測以及對治療效果監(jiān)測有積極意義。第二部分腦白質(zhì)高信號微循環(huán)和微結(jié)構(gòu)改變和認知功能減退相關性的研究WMH與認知功能減退有關,但目前對WMH的認知功能減退患者的大腦微循環(huán)和微結(jié)構(gòu)改變知之甚少。本研究擬采用體素不相干運動(Intravoxel Incoherent Motion,IVIM)技術研究WMH微循環(huán)和微結(jié)構(gòu)改變及其與認知功能的相關性。本研究共招募32例WMH患者入組本研究。研究比較了 WMH區(qū)域(包含室周白質(zhì)高信號 periventricular WMHs,PWMHs 和深部白質(zhì)高信號 deep WMHs,DWMHs)與周邊正常白質(zhì)的IVIM模型重建的快速彌散系數(shù)(D*)、灌注系數(shù)(f)和慢速彌散系數(shù)(D)。采用多變量線性分析確定與認知功能相關的獨立因素。認知功能情況采用簡易精神狀態(tài)檢查表進行評估。研究結(jié)果發(fā)現(xiàn)相對于正常腦白質(zhì)組織,WMH組織D*顯著降低,f值顯著升高,D值顯著升高。只有PWMH中f值是與認知功能MMSE評分獨立相關。本研究提示W(wǎng)MH患者快速彌散系數(shù)D*降低,而慢速彌散系數(shù)D增加;研究還發(fā)現(xiàn)PWMHs灌注系數(shù)f增高與更佳的認知功能有關,此發(fā)現(xiàn)為我們理解WMH患者認知功能減退提供了病理生理基礎。第三部分腦白質(zhì)高信號全腦纖維束損害特征的MRI研究WMH發(fā)生的部位、體積與功能障礙的發(fā)生存在著一定程度的對應關系,目前仍然缺乏針對WMH病變過程中是否存在某些纖維束特異性受損導致不同功能損害,以及不同纖維束之間受損嚴重程度比較的研究。本研究連續(xù)招募125例WMH患者和74例正常對照者。采用約翰霍普金斯大學Brain Mapping的纖維束模板,觀察WMH患者全腦不同纖維束的DTI參數(shù)的改變。研究結(jié)果顯示W(wǎng)MH彌散地影響全腦的纖維束結(jié)構(gòu),所有纖維束均出現(xiàn)FA值下降,MD值升高;其影響范圍遠大于T2FLAIR上所觀察到的高信號區(qū)域;而不同纖維束在病程中受損的情況并不相同,上縱束、額枕束和丘腦前放射等纖維束的結(jié)構(gòu)受到了更加嚴重的損害,未來的研究應該對這些部位的WMH更易導致纖維束受損加以考慮。
[Abstract]:Cerebral white matter hyperintensities (white matter, hyperintensities, WMH) is showed in T2 weighted magnetic resonance imaging or T2 flair, bilateral periventricular and subcortical white matter in multiple punctate, patchy or diffuse high signal. Studies have shown that more than 90% years old people are WMH.WMH in the past is considered to be a normal physiological age-related changes, but recent studies show that WMH is a high risk factor of stroke, dementia, depression and other diseases, the mechanism of the occurrence and development of WMH and its structure and brain function abnormality, has important clinical value in behavior impairment. This study is mainly based on multi modality magnetic magnetic resonance imaging (MRI) technique, using susceptibility weighted imaging, diffusion tensor imaging, intravoxel incoherent motion and other methods, to explore the mechanism of WMH, and the mechanism of WMH in cognitive decline in the main content. The research includes the following three parts: the first part vein source mechanism of cerebral white matter hyperintensities occurred showed cerebral vein collagen fibrosis caused by venous reflux disorder associated with WMH, but the lack of objective evidence. We study in vivo by magnetic resonance imaging to quantify the susceptibility of deep brain ischemia or expansion of medullary veins and the severity of WMH correlation this study. A retrospective analysis of 158 cases of WMH patients and 50 control groups of patients with clinical and laboratory data, on 3TMRI susceptibility weighted imaging method for measuring deep medullary veins voxels with T2 and Flair WMH volume measurement organization (as WMH severity index) were analyzed. Then, linear regression analysis the correlation between Pearson and.WMH deep medullary veins in number of patients was significantly higher than the control group on the voxel correlation quantity and volume of WMH. Deep medullary veins increase in number and whole brain volume and WMH To adjust the number of independent related factors of local lesion age and the volume of the WMH. This study shows that the deep cerebral venous blood deficiency or ischemia play an important role in the pathogenesis of WMH, as predicted in WMH patients and to monitor treatment has a positive meaning. The second part of the brain white matter hyperintensities and micro structure change and microcirculation the cognitive dysfunction of WMH and cognitive function correlation loss related to, but the cognitive function of WMH patients with impaired cerebral microcirculation and micro structure change is poorly understood. In this study we used voxel incoherent motion (Intravoxel Incoherent, Motion, IVIM) WMH technology research of microcirculation and micro structure changes and their relationship with cognitive function. This study recruited 32 patients with WMH were enrolled in this study. The research and comparison of the WMH region (including periventricular white matter hyperintensities on periventricular WMHs, PWMHs and deep white matter Deep signal WMHs, DWMHs) fast diffusion coefficient IVIM model reconstruction and the surrounding normal white matter (D*), the perfusion coefficient (f) and slow diffusion coefficient (D). Analysis using multivariate linear independent factors associated with cognitive function. The cognitive function with mini mental state examination of assessment. Results compared with normal brain white matter tissue, WMH tissue D* decreased significantly, f increased and D values increased significantly. Only in the PWMH F value is independently associated with cognitive function score of MMSE. This study suggests that WMH patients with rapid diffusion coefficient D* decreased, while the slow diffusion coefficient D increases; the study also found that PWMHs perfusion coefficient f correlated with cognitive function better, the findings of cognitive function in patients with WMH provides the pathophysiological basis of loss for us to understand the WMH features of MRI parts. The third part of the brain white matter hyperintensities brain fiber bundle damage body Product and dysfunction is related to a certain extent, there is still a lack of specificity for whether certain fiber bundle damage lead to different functional damage WMH lesions, and between different fiber bundle injury severity of comparison. The study recruited 125 consecutive patients with WMH and 74 normal controls. The fiber bundle template the Johns Hopkins University Brain Mapping, observe the DTI parameters of the whole brain of different fiber bundles with WMH changes. Research results show that the effect of whole brain fiber bundle structure of WMH dispersion, all fiber bundles showed FA decreased, MD value increased; the range of influence is far greater than the high signal area of T2FLAIR on the observed difference; the fiber bundle damage in the course of the disease is not the same, superior longitudinal fasciculus, fronto occipital fasciculus and anterior thalamic radiation structure of fiber bundle has been more serious damage in the future. It should be considered that the WMH of these parts should be more vulnerable to the damage of the fiber bundles.
【學位授予單位】:浙江大學
【學位級別】:博士
【學位授予年份】:2017
【分類號】:R445.2;R741
【相似文獻】
相關期刊論文 前7條
1 張魁忠;涂海洪;劉志禮;樓小亮;柴建勝;張鐵;周榮平;;脊髓型頸椎病MRI-T_2WI高信號與臨床預后分析[J];南方醫(yī)科大學學報;2009年10期
2 傅元芳,李啟權,鐘興,陳金城;MRI腦室四周白質(zhì)高信號的表現(xiàn)及臨床意義[J];中國醫(yī)學影像技術;2000年09期
3 王賀波;張和振;靳瑋;王天俊;郭宗成;馮亞青;李玲;趙大衛(wèi);王建華;呂佩源;;半自動MRI定量方法測定腦白質(zhì)高信號體積與病變定性評分的相關性[J];中國組織工程研究與臨床康復;2009年04期
4 謝林,千葉一裕,金明熙,呂剛,范廣宇;單開門式椎板成形術后核磁共振脊髓內(nèi)T_2加權高信號與運動功能障礙[J];中國臨床康復;2002年02期
5 張曉錦,李優(yōu)偉,唐林;MRI掃描T_1WI呈高信號腦壞死灶1例[J];中國醫(yī)學影像學雜志;2000年02期
6 張鵬;王培鑫;申勇;王林峰;;頸脊髓MRI高信號與神經(jīng)細胞凋亡的相關性研究[J];中國矯形外科雜志;2014年02期
7 ;[J];;年期
相關博士學位論文 前1條
1 孫建忠;腦白質(zhì)高信號的磁共振影像學研究[D];浙江大學;2017年
相關碩士學位論文 前4條
1 杜偉亮;脊髓型頸椎病不同類型MRI T_2WI高信號與患者預后的關系[D];河北醫(yī)科大學;2015年
2 鐘婷婷;顱內(nèi)外動脈粥樣硬化與腦白質(zhì)高信號關系的研究[D];第三軍醫(yī)大學;2016年
3 張鑫;頸髓MRIT2高信號強度及范圍與脊髓型頸椎病臨床表現(xiàn)的相關性研究[D];河北醫(yī)科大學;2011年
4 陳忠華;基于CTA或MRA研究頸內(nèi)動脈狹窄和再通與MRI顱內(nèi)高信號血管征的相關性[D];浙江大學;2014年
,本文編號:1504496
本文鏈接:http://sikaile.net/linchuangyixuelunwen/1504496.html