用户名: 密码: 验证码:
大脑脚FA值及面积相关影响因素以及脑梗死后不同运动诱发电位条件下经颅磁刺激对它们的影响
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
脑梗死可引锥体束的Wallerian变性(简称远隔损害),并对患者的神经功能恢复产生不良影响。然而针对大脑中动脉梗死后而引起的Wallerian变性的研究仅限于与锥体束相关的皮质及白质,在正常人,不同部位的皮质及白质FA值(fractional anisotropy)各异,脑梗死后各部位FA值变化也不一致,造成了对于Walllerian变性状态评估的困难。
     本研究以大脑脚为突破点解决了因同一动脉分布区不同的部位其FA值不同所造成的研究困难,以运动诱发电位为条件解决了同为大脑中动脉分布区脑梗死后体征也不一致,预后也不同所造成的研究困难。首次确定了大脑脚参数的下限值并将其与运动诱发电位相结合对脑梗死后Wallerian变性状态及肢体运动功能进行了评估以及研究了经颅磁刺激对它们的影响。
     脑梗死后Wallerian变性,在早期主要表现为患侧大脑脚FA值的进行性降低,晚期表现为患侧大脑脚萎缩,但在正常情况下大脑脚的FA值及面积本身存在变异,大脑脚的FA值下降什么程度会对肢体的运动功能产生不良影响,什么时间出现大脑脚面积的改变,只有解决了这些问题才能用大脑脚的FA值及面积对脑梗死后Wallerian变性状态做出准确评估。
     运动诱发电位(motor evoked potential, MEP)是反映锥体束功能状态的客观的定量指标,并可以用来推测脑梗死后神经功能恢复情况,运动诱发电位阳性肢体运动功能恢复较好,阴性则预后不佳,脑梗死后在弥散张量成像上可见患侧大脑脚FA值进行性降低,FA值越低Wallerian变性越重,肢体功能恢复越差,脑梗死后Wallerian变性状态及运动诱发电位的变化均取决于原发病灶的程度,部位与所累及锥体束的关系,我们推测大脑脚FA值与运动诱发电位的变化具有一致性,但有研究表明:脑梗死后患大脑脚的FA值在12周内呈进行下降,而肢体运动功能评分却逐渐增加,这会给脑梗死后判断Wallerian状态及肢体运动功能恢复带来不确定性,因此将运动诱发电位与磁共振弥散张量成像结合可以更加准确评估脑梗死后Wallerian变性状态及其预后。
     近几年的研究表明重复经颅磁刺激(TMS)有促进肢体运动功能恢复的作用,其主要是通过增强对脑缺血耐受性,对缺血后再灌注脑损伤的保护,调节神经突触的功能及促进神经突触再生等而起作用,我们推测经颅磁刺激对于脑梗死后大脑脚FA值及面积的变化可能有影响,但其程度如何?具有什么临床意义需进行探讨。
     本研究旨在探讨正常人大脑脚FA值及面积变化特点,建立相应参数,并研究可能累及锥体束的病变对大脑脚相应参数的影响,明确不同运动诱发电位条件下脑梗死后大脑脚FA值及面积变化特点及相应参数的临床意义以及经颅磁刺激对它们的影响,为脑梗死病人治疗及预后评估提供客观有效的方法。
     第一部分正常中国人大脑脚FA值及面积变化的特点
     一研究内容与方法
     研究正常人大脑脚FA值及面积的变异情况,确定大脑脚FA值、FA值偏侧性(双大脑脚FA值不对称比值)、大脑脚面积及大脑脚面积偏侧性的下限值,初步探索年龄对大脑脚各参数的影响及各参数下限值的临床意义。招募的健康自愿者及以非神经系统损害为主诉的住院病人105例,男51例,女54例,按性别分为男性组与女性组,按年龄分为中青年组与老年组,给予常规头MR及DTI扫描,大脑脚FA值及面积的检测分别参照Basser及Mark所使用方法。大脑脚各参数下限值确定采用均数-1.64标准差。
     二结果
     男女2组的年龄,大脑脚FA值、面积及其偏侧性差异无统计学意义。男性及女性左右大脑脚之间FA值及面积差异无统计学意义,中青年组与老年组相比较,大脑脚FA值、面积及其偏侧性无统计学意义,老年组的面积有缩小趋势,大脑脚FA值及其偏侧性下限值分别为0.36及0.77,大脑脚面积及其偏侧性下限值分别为0.84cm2及0.83。
     三小结
     1、我们确定了大脑脚FA值、FA值偏侧性,大脑脚面积及其偏侧性的正常下限值。
     2、年龄对大脑脚FA值及其偏侧性,对大脑脚面积偏侧性的影响不具有统计学意义,老年人大脑脚面积有缩小趋势。
     3、我们所确定的大脑脚参数可以对脑梗死后Wallerian变性状态进行评估。
     第二部分脑白质疏松症大脑脚FA值及面积变化特点
     一研究内容与方法
     探讨不同程度脑白质疏松病人对大脑脚FA值、面积以及他们偏侧性的影响。对照组为第一部分105例受试者,84例脑白质疏松的病人被纳入研究,对其进行常规头MR及DTI扫描并分组,首先按Aharon-pettetz分级分为4组,1级组18例,2级组19例,3级组30例,4级组17例,对此4组病人双大脑脚FA值、面积及其偏侧性值进行比较,其次按其是否可能累及锥体束再次分组,其中1-2级为1组,3到4级为1组,对此两组及正常人组的双大脑脚FA值、面积及其偏侧性值进行比较。
     二结果
     4组的年龄,双大脑脚FA值、面积及其偏侧性差异无统计学意义。双大脑脚FA值及FA值偏侧性双大脑脚面积偏侧性差异无统计学意义,3-4级组的年龄大于对照组(P=0.000),而其大脑脚面积小于对照组(左侧P=0.002,右侧P=0.003)、双大脑脚FA值及其偏侧性、大脑脚面积的偏侧性各组之间差异无统计学意义(P>0.05)。
     三小结
     1、脑白质疏松对大脑脚FA值及其偏侧性以及大脑脚面积偏侧性的影响不具有统计学意义。
     2、正常人大脑脚FA值及其偏侧性,大脑脚面积偏侧性的下限值可用于脑白质疏松病人合并脑梗死后导致的Wallerian变性状态的判定。
     第三部分锥体束行程上无症状性腔隙性脑梗死大脑脚FA值及面积变化特点
     一研究内容与方法
     探讨锥体束行程上无症状性腔隙性脑梗死对大脑脚FA值、面积以及他们偏侧性的影响。选取经核磁共振检查检确诊为锥体束行程上无症状性腔隙性脑梗死病人54例及第一部分的正常人群组105例为研究对象,对其进行头常规MR及DTI检查分别测得其大脑脚FA值及大脑脚面积计算出它们的偏侧性,54例病人按梗死灶累及侧别,分为患侧组及健侧组并与对照组的左侧和右侧大脑脚的FA值、面积及以及他们的偏侧性进行比较。
     二结果
     腔隙性脑梗死组年龄大于对照组(P=0.016),患侧及健侧大脑脚面积小于对照组(双侧P=0.000),FA值及其偏侧性,大脑脚面积偏侧性与对照组相比较无统计学意义,患侧及健侧大脑脚的面积及FA值的比较无统计学意义(P值分别为:P=0.800及P=0.790)。
     三小结
     1、锥体束行程上无症状性腔隙性脑梗死对大脑脚FA值及其偏侧性,对大脑脚面积偏侧性的影响不具有统计学意义。
     2、正常人大脑脚FA值及其偏侧性及大脑脚面积偏侧性下限值可用于无症状性腔隙性脑梗死合并脑梗死后导致的Wallerian变性状态的判定。
     第四部分脑梗死后不同运动诱发电位条件下大脑脚FA值及面积变化的动态研究
     一研究内容与方法
     探索脑梗死后在不同诱发电位条件下大脑脚的FA值及大脑脚面积的变化,并探索大脑脚参数下限值的临床意义,以便更好的评估脑梗死后Wallerian的状态。按标准入组的57例大脑中动脉梗死病人,按可否引出运动诱发电位分为运动诱发电位阴性组、阳性组,在运动诱发电位阴性组按患侧大脑脚FA值最低下限值(0.36)分为2组,<0.36组及≥0.36组,分别在脑梗死后1周内、1个月、3个月、6个月及第12个月进行常规MR及DTI检查并于检查前给予偏瘫肢体Fugl-Meyer(FM)评分,运动诱发电位检查在患者首次检查DTI后24小时内进行。
     二结果
     共57例病人,运动诱发电位阴性组29例,阳性组28例;
     1、运动诱发电位阴性组,不同阶段内健侧大脑脚FA值、健侧大脑脚面积及偏瘫肢体Fugl-Meyer评分相互之间差异无统计学意义。患侧大脑FA值及偏侧性呈进行性下降,不同阶段有差异(P=0.000-0.041),患侧大脑脚面积及大脑脚面积偏侧性在发病后6个月及第12个月与发病3个月内相比较有差异,患侧大脑脚面积(P=0.000~0.002),偏侧性P值为0.000,患侧大脑脚面积及偏侧性于病后6个月及第12个月相比较有差异P值分别为0.013及0.000。
     发病后第3个月到12个月患侧大脑脚FA值≥0.36组FM评分逐渐高于<0.36组(P=0.004~0.044)。
     运动诱发电位阴性组在不同阶段FA值及其偏侧性下限值发生率呈逐渐上升趋势,于病后12个月最高,各阶段均高于诱发电位阳性组及对照组(P=0.000),面积偏侧性小于正常下限值(0.83)发生率增高仅出现在病后6个月及12个月。2、运动诱发电位阳性组,1周内患侧大脑脚FA值及FA值偏侧性高于其它各时间段,P值在0.001~0.030之间,1个月时与其它各时间段相比较无统计学意义,患侧大脑脚FA值在第6个月及第12个月稍有增高趋势。患侧肢体FM评分1周内与其它各时间段相比较有差异P=0.000,1个月时与其它各时间段相比较有差异P=0.000,3个月以后各阶段相互比较无统计学意义。
     3、在不同阶段诱发电位阴性组中患侧大脑脚FA值各阶段低于健侧(P=0.000),而在阳性组中仅于发病后1周内患侧大脑脚FA值与健侧无统计学意义(P=0.410),其余各阶段存在差异(P=0.000~0.001)。
     三小结
     1、患侧大脑脚FA值及其偏侧性变化与诱发电位改变对脑梗死后肢体运动功能的评估具有一致性,诱发电位阴性肢体运动功能恢复差,阳性较佳,FA值越低其预后越差。
     2、诱发电位阴性时可于病后6个月发现有患侧大脑脚面积缩小,以后继续加重。患侧大脑脚FA值及其偏侧性于发病后呈进行性下降,不同阶段FA值及其偏侧性下限值发生率呈逐渐上升趋势,均高于诱发电位阳性组及对照组。
     3、诱发电位阴性且患侧大脑脚FA值小于正常下限值(0.36)提示肢体动能恢复不良。但如≥0.36则肢体运动功能仍有不同程度恢复。
     4、诱发电位阳性时患侧大脑脚FA值发病后1个月内有下降以后基本保持不变。并于病后不出现患侧大脑脚面积的改变。
     第五部分磁刺激对脑梗死后不同运动诱发电位条件下大脑脚FA值及面积变化影响的动态研究。
     一研究内容与方法
     探索经颅磁刺激对脑梗死后不同运动诱发电位条件下对大脑脚FA值及面积变化的影响。55例大脑中动脉梗死的病人,按可否引出运动诱发电位分为运动诱发电位阴性组及阳性组,并给予经颅磁刺激治疗。它们的对照组分别为第四部分中的诱发电位阴性组及阳性组病人;在诱发电位阴性组的病人中,对治疗组及对照组大脑脚FA值及其偏侧性,大脑脚面积偏侧性最低下限值出现率进行比较。对诱发电位阴性的入组病人分别在脑梗死后1周内、1个月、3个月、6个月、12月进行常规MR及DTI检查,而对于诱发电位阳性者仅在病后1周、1个月及3个月时进行,所有病人在检查DTI前对偏瘫肢体给予Fugl-Meyer评分,运动诱发电位检查在患者首次检查DTI后24小时内进行。经颅磁刺激治疗在患者神经病学体征停止进展后48h开始,刺激频率3Hz,100%的磁场输出强度(1.5T),每天治疗时间共20分种,连续10天。
     二结果
     1、运动诱发电位阴性时磁刺激治疗结果治疗组25例,对照组29例。
     3个月时治疗组患侧大脑脚FA值及偏侧性高于对照组(P=0.019,P=0.013),6个月及第12个月时治疗组大脑脚面积及偏侧性大于对照组(P=0.000~0.001),治疗后1个月到12个月治疗组偏瘫肢体FM评分逐渐高于对照组(P=0.008~0.024)。治疗组中患侧大脑脚FA值及FA值偏侧性阶段间相互比较出现差异的时间比对照组晚。患侧大脑脚萎缩时间比对照组延迟,12个月时患侧大脑脚面积及面积偏侧性比以前各段小(P=0.001~0.015)。治疗组FA值及FA值的偏侧性最低下限值的出现率在不同阶段与对照组相比有下降趋势,治疗组大脑脚面积偏侧性低于下限值(0.83)发生率在发病后第6个月及第12个月明显少于对照组(P=0.007,P=0.020)。
     2、运动诱发电位阳性组磁刺激治疗结果
     治疗组30例,对照组28例,治疗组在治疗后第1个月(P=0.022)及第3个月(P=0.003)时患侧FA值高于对照组。治疗组3个月内各阶段大脑脚FA值及FA偏侧性无统计学意义,对照组有差异(P=0.001,P=0.011),治疗组患侧大脑脚FA值仅于发病1个月时低于健侧,而对照组发病后第1个月及第3个月均低于健侧。
     三小结
     小结:1、当运动诱发电位阴性时经颅磁刺激治疗减少部分神经元的Wallerian变性发生,可使部分轻度Wallerian变性的神经元逆转及可延迟脑梗死后Walllerian变性的发生,主要表现为治疗组部分病人肢体FM评分与对照组相比较改善明显,大脑脚面积减小时间延迟。
     2、当运动诱发电位阳性时经颅磁刺激可明显阻止患侧大脑脚FA值的进行性下降仅表现为一过性患侧大脑脚FA值的下降,对偏瘫肢体FM评分无影响。
     3.经颅磁刺激可有减少、逆转或延迟脑梗死后Walllerian变性的发生与发展。
     全文结论
     1.正常人大脑脚FA值下限值为0.36、FA值偏侧性下限值为0.77,大脑脚面积及其偏侧性的正常下限值分别为0.84cm2及0.83。
     2.年龄、脑白质疏松及无症状性腔隙性脑梗死对大脑脚FA值及其偏侧性,大脑脚面积偏侧性影响无统计学意义,但其可使大脑脚面积减小,大脑脚面积在应用时最好采用自身对照。
     3.大脑脚FA值及其偏侧性,大脑脚面积偏侧性下限值可用于脑白质疏松及无症状性腔隙性脑梗死合并脑梗死时,通过大脑脚对Wallerian变性状态评估。
     4.患侧大脑脚FA值及其偏侧性变化与运动诱发电位改变对脑梗死后肢体运动功能的评估具有一致性。
     5.诱发电位阴性时可于病后6个月发生大脑脚萎缩。
     6.运动诱发电位阴性时且患侧大脑脚FA值小于正常下限值(0.36)提示肢体动能恢复不良。但如≥0.36则肢体运动功能仍有不同程度恢复。
     7.经颅磁刺激治疗可有减少、逆转或延迟脑梗死后Walllerian变性的作用。
Wallerian degeneration (remote damage) occurs in pyramidal tract after cerebral infarction, which can produce blight to the restoration of limbs movement. The studies are limited in relative cortex and white matter of pyramidal tract. There are different fractional anisotropy (FA) in different cortex and white matter in normal adults and change in different way after cerebral infarction which bring into difficulties in evaluating the status of Wallerian degeneration.
     The difficulties that there is different FA in different area dominated by middle cerebral artery were overcome through relative study on cerebral peduncles (CP) and the difficulties of different sign and prognosis caused by the different lesion in the area dominated by cerebral middle artery under different conditions of Motor evoked potential (MEP). This is the first study of combining parameters of CP with MEP to evaluate the status of Wallerian degeneration and prognosis of limbs movement and the Transcranial magnetic stimulation (TMS) effect on them.
     FAof CP decreasing progressively is the sign of Wallerian degeneration after cerebral infarction in early stage and cerebral peduncle atrophy in late stage, but how the FA and area of CP change in normal adults? What degree the FA decreasing can product blight to the restoration of limbs movement after cerebral infarction? what time do the area atrophy of CP appear? Only these problem solved does the status of Wallerian degeneration be evaluated accurately. MEP(motor evoked potential) is quantity indice of evaluating the function status of cortical spinal tract which can be used to evaluate the integrity and function recovery of corticospinal tract following stroke, Positive MEP predict better recovery of limbs movement which is reversed in negative MEP. Cerebral infarction can result in Wallerian degeneration, the more severe Wallerian degeneration the more FA decreased on Diffusion tensor imaging (DTI) and the worse restoration of limbs movement, but the extent of Wallerian degeneration and the variance of MEP after stroke depend on the extent of the primary lesion and its location in relation to the affected fibre tracts,We presume that there is coherence change between FA and MEP, but FA decreased progressively after cerebral infarction and scores of limbs movement increased gradually were shown on some paper, which brought indetermination in evaluating the status of Wallerian degeneration and restoration of limb movement. The status evaluation of Wallerian degeneration and prognosis after cerebral infarction can be done more accurately by combining MEP with DTI.
     Transcranial magnetic stimulation (TMS) can accelerate the restoration of limb movement through increasing endurance to ischemia of brain, brain damage protection caused by re-perfusion, regulating the function of synapse and facilitating the regeneration of nerve synapse. We presume that there can be effect of the TMS on the FA and area changes of CP after cerebral infarction. But what is the degree of the effect of TMS on them? What clinical significance is there needed to be explored.
     The aim of the study is to explore the variation characteristics of FA and area of CP in normal adults and to build up relative parameters and to study the effect of involving pyramidal tract possibly on FA and area of CP, to know characteristics of FA and area changes of CP after cerebral infarction and relative parameters clinical significance under different MEP condition and the TMS effect on them, to provide impersonality and efficacy methods for evaluating the prognosis and treatment efficacy after cerebral infarction.
     PartⅠThe Study of the Fractional anisotropy, Area, and Their Asymmetry of the cerebral peduncles in Normal Chinese Adults
     Contents and methods:
     To study the range of variation of fractional anisotropy (FA) and area of the CPs and to confirm the lower limited values of FA, area of cerebral peduncle (CP) and their Asymmetry,to explore the age effect on them and their clinical significance primarily.
     105 normal people took part in this study (51 male,54 female), they were divided into two groups according to gender (male group and female group),they were divided into young and middle age group and aging group according to age.standard MRI examination and diffusion tensor imaging (DTI) were performed. FA and area were confrimed by Basser and Mark methods.The lower limited values of the CP parameters were comfirmed by the mean-1.64 standard deviation(SD).
     Results:
     There was no differecne of age,FA,area and their assymmentry between male and female group and between young-middle age group and aging group too, there was tendency of cerebral peduncle area being smaller in aging group.there was no differecne of FA,area between thte left and rihgt CP. The lower limit for FA was 0.36 and assymmetry ratio 0.77. The lower limit of the area was 0.84 cm2 and 0.83 for its symmentry.
     Summary:
     1.We have established the lower limited values of normal variation of the CPs for FA, area and their asymmetry ratio.
     2. There was no effect of age on FA, area and their asymmentry ratio, but there was tendency of area being smaller in aging group.
     3.The parameters of CPs confirmed can be used to evaluate the status of Wallerian degeneration after cerebral infarction.
     PartⅡThe Characteristic and Significance of Fractional anisotropy and Area Changes in CPs among Leukoaraiosis patients
     Contents and methods:
     To research the effect of Leukoaraiosis (LA) in different degrees on the FA, area and their asymmetry of CPs. Control group was consisted of 105 cases in the first part, 84 LA patients who were grouped took part in this study and stand MR and DTI were performed among them. First they were divided into 4 groups according to Aharon-pettetz (grade 1 group=18,grade2 group=19,grade 3 group=30,grade 4group=17). The FA and area and their asymmetry were compared between groups, then they were grouped into two groups (grade 1-2 group, grade 3-4 group) according to whether the pyramidal tract might be involved, FA, area and their asymmetry were compared between 2 groups and control group.
     Results:
     There was no difference in age, FA and area of CP and their asymmetry between 4 groups among 84 patients. There was tendency of the area of CP being smaller in grade 3-4group. The area of both side were smaller than control group (left P=0.002,P=0.003 in right), the age of grade 3-4group was older than control group. There was no difference of FA and FA asymmetry and area asymmetry between grade 3-4group and control group.
     Summary:
     1.There was no effect of LA patients on FA and FA asymmetry and area asymmetry.
     2.The lower limited value of FA and FA asymmetry and area asymmetry in normal adults can be used for evaluating the Wallerian status after cerebral infarction among patients with LA.
     PartⅢThe Characteristic and Significance of Fractional anisotropy and Area of CPs among Patients with Silent Lacunar Infarct in Pyramidal Tract
     Contents and methods:
     To research the effect of silent lacunar infarct in pyramidal tract on FA and area and their asymmetry of pyramidal tract.54 patients with silent lacunar infarct in pyramidal tract diagnosed by MRI and 105 healthy adults in first part were selected as study subjects, DTI were performed and their FA and area of CP and their asymmetry were measured and calculated. The CP FA and area of 54 patients were divided into two group according to injured side of CP which were injured side group and uninjured side group, both FA and area of injured side group and uninjured side group were compared with the control group, the CP FA and area asymmetry of lacunar infarct group was compared with the control group.
     Results:
     The age of lacunar infarct group was older than control group, The CP areas of 54 patients with silent lacunar infarct in pyramidal tract were smaller than control group(both Left and right P=0.000). There was no difference of CP FA and asymmetry and area asymmetry between observed group and control group, there was no difference of FA and area between left and right CP in lacunar infarct group (t=0.254 P=0.800,t=0.268 P=0.790).
     Summary:
     1.There was no effect of silent lacunar infarct in pyramidal tract on FA and FA asymmetry and area asymmetry.
     2.The lower limited value of FA and FA asymmetry and area asymmetry in normal adults can be used for evaluating the Wallerian status after cerebral infarction among patients with silent lacunar infarct.
     Part IV The Following up study of FA and area changes of CP After Cerebral Infarction under different Motor Evoked Potential condition
     Contents and methods:
     The aim is to study the FA and area change of CP under different condition of motor evoked potential (MEP) and to evaluate the status of Wallerian after cerebral infarction.
     57 patients with cerebral middle artery infarction were studied and were divided into two groups according to absence and presence of MEP, negative group(MEP-) and positive group(MEP+).Two groups were divided in MEP-group according to the lower limited value (group<0.36 and≥0.36 group),stand MR and DTI of patients were performed in first week,first month,third month,6th month,and 12th month,and Fugl-Meyer score was done. The MEP was performed in 24 hours at first week after cerebral infarction.
     Results:
     There were 57 patients in all, MEP- group 29cases, MEP+ 28 cases.
     1.The result of MEP- group:There were no difference of FA and area in healthy side of CP and there was no difference of Fugl-Meyer scores between different periods. FA and asymmetry decreased progressively,there was difference between different periods (P=0.000~0.041). The area and area asymmetry were smaller in 6th month (P=0.002) and 12th month (P=0.000) than the first week after cerebral infarction. Fugl-Meyer Scores in FA equal to or higher than 0.36 patients were higher than those in lower than 0.36 gradually from the third month to 12th month (third month p=0.044,6th month P=0.041,12th month P=0.004). There was increased tendency of occurrence rate of lower limited value in FA and FA asymmetry during different period which reached the highest at 12th month in MEP-group, which were higher than in MEP+ and control group (P=0.000). Occurrence rate of lower limited value of CP area asymmetry occurred in 6th month and 12th month only (P=0.000).
     2.MEP+ group:FA and FA asymmetry after stroke for the first week were higher than those in each period till 12th month (P=0.001~0.030), there was no difference of FA and FA asymmetry in the first month compared with other period. The FM scores were lower in the first week than the other period (P=0.000) and the FM scores in first month were lower than the third to 12th month (P=0.000). There was no difference of FM scores in third month than 6th month and 12th month.
     3.FA of CP in lesion side in MEP- group were lower than contralateral side through all periods, there was no difference between CP of lesion side and contraleteral side in first week (P=0.0410), there was difference between healthy side and lesion side from the first month to 12th month.
     Summary:
     1.There was consistency of FA and FA asymmetry in evaluating the restoration of limb movement with MEP after cerebral infarction, worse restoration of limb movement in MEP-group and reverse in MEP+ group. The lower FA and FA asymmetry were the worse the prognosis.
     2.It was found that the area of CP became smaller in the 6th month. FA of CP in lesion side and FA asymmetry decreased progressively in MEP- group, the occurrence rate of lower limited value of FA and FA asymmetry appeared in rising tendency from beginning to the 12th month which were higher than MEP+group and control group.
     3.If the FA value were smaller than normal lower limited value (0.36) the movement function of limb got worse restoration, or it could get better restoration to some degree in MEP-group.
     4.The FA of CP decreased within the first month and would keep unchangeable from third month to 12 month. There was no change on area of CP from beginning to the 12th month after stroke in MEP+ group.
     PartⅤThe Following up Study of the Effect of Transcranial magnetic stimulation on FA and Area changes of CP After Cerebral Infarction under Different Motor evoked potential Condition
     Content and methods:
     To Study the effect of transcranial magnetic stimulation (TMS) on FA and area changes of CP after cerebral infarction under different motor evoked potential conditions.55 patients with cerebral middle artery infarction were divided into two groups according to absence and presence of MEP, negative group (MEP-) and positive group (MEP+), control group were MEP- and MEP+ group patient in the fourth part. TMS were given to practice patients, occurrence ratio of the FA and FA asymmetry, area asymmetry lower than lower limited values were compared in MEP-patients during different period. Stand MR and DTI were performed among patients in the first week, the first month, the third month,6th month, and 12th month and Fugl-Meyer score was done at the same time in MEP- patients and the MEP was performed in 24 hours at the first week after cerebral infarction, only first week and month and the third month was the study performed in MEP+ patints in the same way. The transcranial magnetic stimulation was given after the neurologic sigh stoped progressing in 48 hours. The parameters were as following:frequency 3Hz,100% output(1.5T),20 minutes a day,continuing for 10 days.
     Results:
     1. The result of MEP- group 54 cases, practice group 25,control group 29 cases.
     The FA and FAasymmetry in practice group were higher than control group in the third month (P=0.019,P=0.013).The area and area asymmetry of CP were higher than control group in 6th and 12th month (P=0.001,P=0.000). Fugl-Meyer scores in practice group were being higher gradually than control group from the first month to 12th month(P=0.008-0.024).The was no difference of FA and FA asymmetry in practice group between the first week and first month,which were higher in the first month than 6th month and 12th month.The area and area asymmetry in 12th month were smaller than previous period (P=0.001-0.015). There were decreased tendency of the FA and FA asymmetry lower than lower limited values occurrence ratio compared with control group. Area asymmetry lower than lower limited values occurrence ratio decreased in 6th and 12th month (P=0.007,P=0.020).
     2. The result of MEP+ group
     58 cases, practice group 30 and control group 28.The FA of CP in lesion side was higher than control group in the first month (P=0.022) and the third month (P=0.003). There was no difference of FA and FA asymmetry in practice group between periods in 3month,there was difference in control group (P=0.001,P=0.0110). There was phenomenon of FA and FA asymmetry decreased in 3month while there was no such phenomenon in practice group. FA in lesion side were lower than healthy side only in the first month which were decreased in first month and third month in control group.
     Summary:
     1. TMS can decrease, reverse or prolong Wallerian degeneration occurrence, which was shown on FM score increased and CP atrophy was deleyed to the 12th month in MEP- group.
     2. TMS can stop FA of CP in lesion side decreasing progressively which was shown on FA of CP in lesion side decreasing temporarily in practice MEP+ group.
     3. TMS can decrease, reverse or prolong Wallerian degeneration occurrenc.
     Conclusion:
     1. The lower limit for FA was 0.36 and assymmetry ratio 0.77. The lower limit of the area was 0.84 cm2 and 0.83 for its symmentry ratio in normal adults.
     2. There is no effect of age, leukoaraiosis and silent lacunar infarct on FA and assymmetry ratio and area asymmetry.
     3. The lower limited value of FA and FA asymmetry and area asymmetry in normal adults can be used for evaluating the Wallerian status after cerebral infarction among patients with LA and silent lacunar infarct.
     4. There is consistency of FA and FA asymmetry in evaluating the restoration of limb movement with MEP after cerebral infarction.
     5. The areas of CP become smaller in the 6th month after cerebral infarction in MEP-group.
     6. If the FA value were smaller than normal lower limited value (0.36) the movement function of limb got worse restoration, or it could get better restoration to some degree in MEP- group.
     7. TMS can decrease, reverse or prolong Wallerian degeneration occurrenc after cerebral infarction.
引文
[1]梁志坚.脑梗死后远隔部位继发性损害的影像学诊断及其临床意义[J].国际脑血管病杂志,2008,16(4):293-295.
    [2]Marcel Dihne.Different Mechanisms of Secondary Neuronal Damage inThalamic Nuclei After Focal Cerebral Ischemia in Rats[J]. Stroke 2002,33:3006-3011.
    [3]Yu C,Zhu C,Zhang Y.et al. A longitudinal diffusion tensor imaging study on Wallerian degeneration of cortical spinal tract after motor pathway stroke[J].Neuroimage,2009,47(2):451-458.
    [4]梁志坚.磁共振弥散张量成像动态观察脑梗死后继发锥体束损害[J].中国神经精神杂志,2007,33(3):159-161.
    [5]梁志坚.脑桥梗死后相关神经纤维继发性损害的DTI研究及其意义[J].中国神经精神杂志,2008,34(3):139-144.
    [6]Joshua S, Robert C, Erbil A. Quantitative Diffusion-tensor Anisotropy Brain MR Imaging: Normative Human Data and Anatomic Analysis[J]. Radiology,1999,21 (3):770-784.
    [7]Kaori F,Masafumi H,Masako M et al. Regional changes of farctional anisotropy with normal aging using statistical parametric mapping(SPM) [J].The Journal of Medical Investigation,2005,52(8):186-190
    [8]David JW,ahmed TT,Christopher AC, etal. Diffusion tensor imaging can detect and quantify corticospinal tract degeneration after stroke[J]. J Neurol Neurosurg Psychiatry, 2000,69:269-272.
    [9]Pratik M,Mark M,Robert C et al. Differences between GrayMatter and White MatterWater Diffusion in Stroke:Diffusion-Tensor MR Imaging in 12 Patients[J]. Radiology, 2000,215(1):211-220.
    [10]Mark,E. Taub,C. Perkins et al. Poststroke Cerebral Peduncular Atrophy Correlates with a Measure of Corticospinal TractInjury in the Cerebral Hemisphere[J]. Am J Neuroradiol,2008,29:354-358.
    [11]Kuhn MJ,Mikulis DJ,Ayoub DM,et al.Wallerian degeneration after cerebral infarction evaluation with sequential MR imaging[J].Radiology,1989,172:179-182.
    [12]王强,崔利华,张通.脑卒中后Wallerian变性和康复预后相关性研究进展[J].中国康复理论与实践,2007,11(13):1036-1038.
    [13]Pennisi G, Rapisarda G, Bella R, et al. Absence of response to early transcranial magnetic stimulation in ischemic stroke patients:prognostic value for hand motor recovery[J]. Stroke,1999,30(12):2666-2670.
    [14]Thomalla G,Glauche V,Weiller C et al.Time course of wallerian degeneration after ischaemic stroke revealed by diffusion tensor imaging[J]. Neurol Neurosurg Psychiatry,2005,76:266-268.
    [15]邢岩.经颅磁刺激技术在缺血性脑血管病中的研究进展[J].国际神经病学神经外科学杂志,2007,34(1):64-66.
    [1]Poupon C, Mangin J, Clark CA, et al. Towards inference of human brain conneetivity from MR diffusion tensor data[J]. Med Image Anal,2001,15(1)11-15.
    [2]Beauliue C.The basis of anisotropic water diffusion in the nervous system- a technical review[J].NMR Biomed,2002,15:435-455
    [3]梁志坚.脑梗死后远隔部位继发性损害的影像学诊断及其临床意义.国际脑血管病杂志[J],2008,16(4):293-295.
    [4]Mark VW, Taub E, Perkins C, et al.Poststroke Cerebral Peduncular Atrophy Correlates with a Measure of Corticospinal Tract Injury in the Cerebral Hemisphere[J]. Am J Neuroradiol,2008,29:354-358.
    [5]Helenius J,Soinne L,Perkio J,et al. Diffusion-weighted MR imaging in normal human brains in various age groups[J].AJNR,2002,23(2):194-199
    [6]Basser PJ, Pierpaoli C. Micro structural and physiological features of tissues elucidated by quantitative-diffusion-tenso MRI[J].J Mag Reson B,1996,111:209-219.
    [7]M(?)ller M, Frandsen J, Andersen G,et al.Dynamic changes in corticospinal tracts after stroke detected by fibretracking[J]. J Neurol Neurosurg Psychiatry, 2007,78:587-592.
    [8]Cendes F,Leproux F, Melanson D, et al. MRI of amygdala and hippocampus in temporal lobe epilepsy [J]. J Comput Assist Tomogr,1993,17(2):206-210.
    [9]Joshua S, Robert C, Erbil A. Quantitative Diffusion-tensor Anisotropy Brain MR Imaging:Normative Human Data and Anatomic Analysis [J].Radiology, 1999,21(3):770-784.
    [10]Kaori F,Masafumi H,Masako M et al. Regional changes of farctional anisotropy with normal aging using statistical parametric mapping(SPM) [J].The Journal of Medical Investigation,2005,52(8):186-190
    [11]David JW,ahmed TT,Christopher AC, etal. Diffusion tensor imaging can detect and quantify corticospinal tract degeneration after stroke [J]. J Neurol Neurosurg Psychiatry,2000,69:269-272.
    [12]Pratik M,Mark M,Robert C,et al. Differences between GrayMatter and White Matter Water Diffusion in Stroke:Diffusion-Tensor MR Imaging in 12 Patients[J]. Radiology,2000,215(1):211-220.
    [13]梁志坚,刘斯润,曾进胜等.磁共振弥散张量成像动态观察脑梗死后继发锥体束损害[J].中国神经精神疾病杂志,2007,33(3):159-163.
    [14]Wen GQ. Diagnostic value of diffusion tensor magnetic resonance imaging in patients with cerebral infarction [J]. Chin J Cerebravasc Dis 2006,3:450-453.
    [15]Yoshiura T, Wu O, Zaheer A, et al. Highly diffusion—sensitized MRI of brain: dissociation of gray and white matter[J].Magn Reson Med,2001,45:734-740.
    [16]凌雪英,王秀河,刘斯润.磁共振弥散张量成像对正常成年人胼胝体性别差异的初步研究[J].中国临床解剖学杂志,2005,53(1):53-55.
    [17]Zhang YT,Zhang CY, Zhang J.Age related changes of normal adult brain structure:analyse with diffusion tensor imaging[J]. Chinese Medical Juournal, 2005,118(13):1059-1065.
    [18]张卫东,梁碧玲,叶瑞心等.年龄对正常成人脑弥散特性影响的初步研究[J].中国医学影像学杂志,2005,13(5):336-338.
    [19]Kuhn MJ,Mikulis DJ,Ayoub DM,et al.Wallerian degeneration after cerebral infarction evaluation with sequential MR imaging[J].Radiology,1989,172:179-182.
    [20]王强,崔利华,张通.脑卒中后Wallerian变性和康复预后相关性研究进展[J].中国康复理论与实践2007,11(13):1036-1038.
    [21]方珉.卒中后皮质脊髓束Waller变性的DTI表现及其与运动功能受损的关系[J],国际脑血管疾病,2009,17(3),205-210.
    [22]曾庆师,李李传福,刘尊齐等.正常人脑体积随年龄变化的磁共振成像定量分析[J].中国医学科学院报,2006,12:795-798.
    [23]祁光蕊,陈楠,郭玉林等.中国汉族成人岛叶体积与年龄的相关性研究[J].实用放射学杂志,2010,609-631.
    [24]Gurol ME,Irizarry MC, Smith EE, et al. Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy[J]. Neurology,2006, 66:23-29.
    [1]钟维佳,赵建农,谢微波等.脑自质稀疏症的MR弥散张量成像研究[J].重庆医科大学学报,2008,33(2):198-202.
    [2]梁志坚.脑梗死后远隔部位继发性损害的影像学诊断及其临床意义[J],国际脑血管病杂志,2008,16(4):293-295.
    [3]Mark V W, Taub E, Perkins C et al. Poststroke Cerebral Peduncular AtrophyCorrelates with a Measure of Corticospinal Tract Injury in the Cerebral Hemisphere[J]. Am J Neuroradiol 2008:29:354-358.
    [4]王晨,高培毅,林燕等.脑白质疏松的研究进展[J].中华老年心脑血管病杂志.2008,10(10),797-798
    [5]Sullivan M, Morris R, Huckstep B. Diffusion tensor MRI correlates with executive
    dysfunction in patients with ischaemic leukoaraiosis[J]. J Neurol Neurosurg Psychiatry,2004,75:441-447.
    [6]张卫东,梁碧玲,叶瑞心等.年龄对正常成人脑弥散特性影响的初步研究[J].中国医学影像学杂志,2005,13(5):336-338.
    [7]张雪宁,张云亭.脑白质疏松的扩散张量成像研究[J].临床放射学杂,2006,25(7):593-596
    [8]Della Nave R. Foresti S. Pratesi A. Whole-Brain Histogram and Voxel-Based Analyses of Diffusion Tensor Imaging in Patients with Leukoaraiosis: Correlation with Motor and Cognitive Impairment [J]. AJNR Am J Neuroradiol,2007,28:1313-19
    [9]Pierpaoli C, Barnett A, Pajevic S, etal. water diffusion changes in Wallerian degeneration and their dependence on white matter architecture[J]. Neuroimage,2001,13:1174-1185.
    [10]Thomalla G,Glauche V, Koch MA et al. Diffusion tensor imaging detects early Wallerian degeneration of the pyramidal tract after ischemic stroke[J]. Neuroimage,2004,22:1767-1774
    [11]Thomalla G, Glauche V, Weiller C et al. Time course of wallerian degeneration after ischaemic stroke revealed by diffusion tensor imaging[J]. Neurol Neurosurg Psychiatry,2005,76:266-268
    [12]Velandai S, Richard B, Leigh B, Cerebral White Matter Lesions, Gait, and the Risk of Incident Falls A Prospective Population-Based Study[J].Stroke, 2009,40(1)175-180.
    [13]王敏,曹秉振.脑白质疏松[J].国际脑血管疾病杂志.2006,14(3):219-223
    [14]Pantoni L. Inzitari D. New clinical relevance of leukoaraiosis. European Task Force on Age—Related WhiteMatter-Changes[J]. Stroke,1998,29(2): 543.
    [15]Munoz DG. Leukoaraiosis and ischemia:beyond the myth [J]. Stroke,2006, 37(6):1348-1349.
    [16]苏中华,成义仁,王贵山.首发偏执型精神分裂症患者的脑白质磁共振弥散张量成像研究.中国神经精神疾病杂志,2010,36(4):233-236
    [17]任力杰,陆兵勋,吴明祥.抑郁症患者的认知功能、事件相关电位P300和MR扩散张量成像研究[J].中华神经科杂志,2010,9(5):512-516.
    [18]陈雯洁.老年人认知功能障碍与代谢综合征及其组分相关性分析[J]复旦大学学位论文,2006,5.
    [19]曾庆师.正常人成年脑体积随年龄变化的磁共振成像定量分析[J].中国医学科学院院报,2006,28(6):795-798
    [20]Wahlund L, Barkhof F, Fazekas F, A New Rating Scale for Age-Related White Matter Changes Applicable to MRI and CT[J].Stroke,2001,32(6):1318-1322
    [21]Tom J, Philip A, Alexa B,et al. Stroke Risk Profile Predicts White Matter Hyperintensity Volume The Framingham Study [J]. Stroke,2004,35(8):1857-1861
    [22]Clifford R, Peter C, Daniel et al. FLAIR Histogram Segmentation for Measurement of Leukoaraiosis Volume[J]. J Magn Reson Imaging.2001,14(6):668-676.
    [23]Schmidt R, Ropele S, Enzinger C,et al. White matter lesion progression, brain atrophy, and cognitive decline:the Austrian stroke prevention study[J]. Ann Neurol,2005,58(4):610-616
    [24]Gurol ME,Irizarry MC, Smith EE, et al. Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy[J]. Neurology,2006, 66:23-29.
    [25]Altaf N, Daniels L,Morgan PS, et al. Cerebral white matter hyperintense lesions are associated with unstable carotid plaques[J]. Eur J Vasc Endovasc Surg.2006,31(1):8-13
    [1]张向前,陆兵勋,刘振华等.腔隙性脑梗死形似正常区的白质损害与超敏C反应蛋白的关系[J].中华神经医学杂志,2009,8(4):380-384.
    [2]中华神经科学会,中华神经外科学会.各类脑血管疾病诊断要点[J].中华神经科杂志,1996,29(6):379-380.
    [3]Price TR, Manolio TA, Kronmal RA, et al. Silent brain infarction On magnetic abnomalitiesin community-dwelling older adults,the cardiovascular heaIth study[J]. Stroke,1997,28(8): 1158-1160.
    [4]Herderschee D, Hijdra A, Algra A, et al. Silent in patients with transient ischemic or minor ischemic stroke[J]. Stroke,1992,23(6):1220-1222.
    [5]Thomalla G,Glauche V,Koch MA et al.Diffusion tensor imaging detects early Wallerian degeneration of the pyramidal tract after ischemic stroke[J].Neuroimage,2004,22:1767-1774.
    [6]Thomalla G, Glauche V, Weiller C etal. Time course of Wallerian degeneration after ischaemic stroke revealed by diffusion tensor imaging[J]. J Neurol Neurosurg Psychiatry,2005,76:266-268.
    [7]Pierpaoli C,Barnett A, Pajevic S, etal. Water diffusion changes in Wallerian degeneration and their dependence on white matter architecture[J].Neuroimage,2001,13:1174-1185.
    [8]Werring DJ, Toosy AT,Clark CA et al. Diffusion tensor imaging can detect and quantify conicospinal tract degeneration after stroke[J]. J Neurol Neurosurg Psychiatry,2000,69:269-272.
    [9]Herderchee[J].Silent stroke. heart dis stroke,1993,2(4),343-345
    [10]Kaori M, Taku H, Hidetaka H et al. Silent Cerebral Infarction is Associated with Incident Stroke and TIA Independent of Carotid Intima-Media Thickness[J].Internal medicine,2010,817-822.
    [11]Jae-Sung L,Hyung-Min K. Risk of "silent stroke" in patients older than 60 years:risk assessment and clinical perspectives[J]. Clinical Interventions in Aging,2010,5:239-251.
    [12]Jae-sung L,Hyung-min K.R.Risk of silent stroke in patients older than 60 years:risk assessment and clinical perspectives[J].Clinical Interventions in Aging,2010,5:239-251.
    [13]Sudha S,Philip A,Alexa S.et al.Association of plasma homocysteine levels with subclinical brain injury:cerebral volumes,white matter hyperintensity and silent brain infarcts on vometric MRI in the Framingham offspring study[J].Arch neurol.2008,65(5):642-649.
    [14]Catherine L,Joel H,Andrew J.et al. Subcortical lacunes are associated with executive dysfunction in cognitively normal elderly [J]. Stroke,2008,39(2):397-402.
    [15]曾庆师.正常人成年脑体积随年龄变化的磁共振成像定量分析[J].中国医学科学院院报,2006,28(6):795-798.
    [16]Gurol ME,Irizarry MC, Smith EE, et al. Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy [J]. Neurology,2006,66:23-29.
    [17]Mark VW, Taub E, Perkins C, et al. Poststroke cerebral peduncular atrophy correlates with a measure of corticospinal tract injury in the cerebral hemisphere[J]. Am J Neuroradiol,2008, 29(2):354-358.
    [1]Thanh G,Geoffery A,Velandai S.et al.Heterogeneity in infarct patterns and clinical outcomes following internal carotid artery occlusion[J].A rch Neurol,2009,66(12):1523-1528.
    [2]Pennisi G, Rapisarda G, Bella R, et al. Absence of response to early transcranial magnetic stimulation in ischemic stroke patients:prognostic value for hand motor recovery[J]. Stroke 1999,30(12):2666-2670.
    [3]Heald A, Bates D, Cartlidge N, et al. Longitudinal study of cerebral motor conduction time following stroke.2. Central motor conduction measured within 72h after stroke as a predictor of functional outcome at 12 months[J]. Brain,1993,116(PT6):1371-1385.
    [4]Michael A, Leonardo G. Contribution of transcranial magnetic stimulation to the understanding of mechanisms of functional recovery after stroke [J]. Neurorehabil Neural Repair,2010,24(2):125-135.
    [5]Poupon C, Mangin J, Clark CA, et al. Towards inference of human brain conneetivity from MR diffusion tensor data[J]. Med Image Anal,2001,15(1)11-15.
    [6]Beauliue C.The basis of anisotropic water diffusion in the nervous system- a technical review[J].NMR Biomed,2002,15:435-455
    [7]梁志坚.磁共振弥散张量成像动态观察脑梗死后继发锥体束损害[J].中国神经精神杂志,2007,33(3):159-161.
    [8]Thomalla QGlauche V,Weiller C et al.Time course of wallerian degeneration after ischaemic stroke revealed by diffusion tensor imaging[J]. Neurol Neurosurg Psychiatry, 2005,76:266-268.
    [9]王强.崔利华.张通.脑卒中后Wallerian变性和康复预后相关性研究进展[J].中国康复理论与实践,2007,11(13):1036-1038.
    [10]Cathy M, Alan B,Peter R et al.Functional potential in chronic stroke patients depends on corticospinal tract integrity[J]. Brain 2007,130:170-180.
    [11]Arac N,Sagduyu A,Binai S,et al. Prognostic value of transcranial magnetic stimulation in acute stroke[J]. Stroke,1995,269(10):162-163
    [12]Khong P,Zhou L,Ooi G,et al.The evaluation of Wallerian degeneration in chronic peaediatric middle cerebral artery infarction using diffusion tensor MR imaging[J]. Cerebravasc Dis,2004,18(3):240-247.
    [13]Kuhn MJ,Mikulis,DJ,Ayoub DM,et al.Wallerian degeneration after cerebral infarction evaluation with sequential MR imaging[J].Radiology,1989,172:179-182.
    [14]Lian L, PhD1, Quan J, Guangliang D. MRI identification of white matter reorganization enhanced by erythropoietin treatment in a rat model of focal ischemia[J]. Stroke,2009, 40(3):936-941.
    [15]Duncan PW, Goldstein LB, Matchar D, Divine GW, Feussner J. Measurement of motor recovery after stroke:outcome assessment and sample size requirements[J]. Stroke.1992;23:1084-1089.
    [16]Duncan PW, Goldstein LB, Homer RD, Landsman PB, Samsa GP,Matchar DB. Similar motor recovery of upper and lower extremities afterstroke[J]. Stroke.1994;25:1181-1188.
    [17]Bonita R, Beaglehole R. Recovery of motor function after stroke[J]. Stroke. 1988;19:1497-1500.
    [18]Mark VW, Taub E, Perkins C, et al.Poststroke Cerebral Peduncular AtrophyCorrelates with a Measure of Corticospinal Tract Injury in the Cerebral Hemisphere[J]. Am J Neuroradiol,2008,29:354-358.
    [19]Khong PL, Zhou LJ, Ooi GC, et al. The evaluation of wallerian degeneration in chronic paediatric middle cerebral artery infarction using diffusion tensor MR imaging. Cerebrovasc Dis,2004,18:240-247.
    [1]Michael A., Leonardo G. Contribution of transcranial magnetic stimulation to the understanding of mechanisms of functional recovery after stroke[J]. Neurorehabil Neural Repair,2010,24(2):125-135.
    [2]邢岩.经颅磁刺激技术在缺血性脑血管病中的研究进展[J].国际神经病学神经外科学杂志,2007,34(1):64-67.
    [3]梁志坚.脑梗死后远隔部位继发性损害的影像学诊断及其临床意义[J],国际脑血管病杂志,2008,16(4):293-295.
    [4]梁志坚,磁共振弥散张量成像动态观察脑梗死后继发锥体束损害[J].中国神经精神杂志,2007,33(3):159-161.
    [5]Khedr E,Ahmed M,Fathy N,et al.Therapeutic trial of repetitive transcranial magnetic stimulation after acute ischemic stroke[J].Neurology,2005,65:466-468.
    [6]Kim Y,You S,Ko M,et al.Repetitive transcranial magnetic stimulation-induced corticomotor excitability and associated motor skill acquisition in chronic stroke[J].Stroke,2006,37:1471-1476
    [7]Speer AM, Khnbrell TA, WasseHnann EM, et al Opposite effects of high and low frequency rTMS on regional brain activity in depressed patients [J]. Biol Psychiatry,2000,48(12): 1133-1141.
    [8]Ziemann U,Muellabcher W,Hallett M,et al. Modulation of practice-dependent plasticity in human motor cortex[J].Brain,2001,124:1171-1181.
    [9]Pennisi G, Rapisarda G, Bella R, et al. Absence of response to early transcranial magnetic stimulation in ischemic stroke patients:prognosticvalue for hand motor recovery[J]. Stroke1999,30(12):2666-2670.
    [10]王强.崔利华.张通.脑卒中后Wallerian变性和康复预后相关性研究进展[J].中国康复理论与实践,2007,11(13):1036-103
    [11]Sander D,Meyer B,Roricht S.et al. Effect of hemisphere-selective repetitive magnetic brain stimulation on middle cerebral artery blood flow velocity [J].Electgroencephalgraphy Clin.Neurophysiol,1995,97(1):43-48.
    [12]张彩元.沈钧康.赵合庆.磁共振弥散加权成像评价局灶性脑缺血大鼠经颅磁刺激后的疗效[J].中国医学影像技术,2009,25(4):567-570.
    [13]Kim YH, You SH, Ko MH, et al. Repetitive transcranial magnetic stimulation-induced corticomotor excitability and associated motor skill acquisition in chronic stroke[J]. Stroke, 2006,37(6):1471-1476.
    [14]郑安洁.程焱.重复经颅磁刺激在脑梗死后运动康复中的应用[J].国际脑血管疾病,2007,15(10):749-752.
    [15]Thomalla QGlauche V,Koch MA et al.Diffusion tensor imaging detects early Wallerian degeneration of the pyramidal tract after ischemic stroke[J].Neuroimage,2004;22:1767-1774.
    [16]Kuhn MJ,Mikulis,DJ,Ayoub DM,et al.Wallerian degeneration after cerebral infarction evaluation with sequential MR imaging[J].Radiology,1989,172:179-182.
    [17]Zijden J, Toorn A, Marel K, et al. Longitudinal in vivo MRI of alterations in perilesional tissue after transient ischemic stroke in rats. Exp Neurol 2008;212:207-212.
    [18]Ding G, Jiang Q, Li L, Zhang L, Zhang ZG, Ledbetter KA, Panda S, Davarani SP, Athiraman H, Li Q, et al. Magnetic resonance imaging investigation of axonal remodeling and angiogenesis after embolic stroke in sildenafil-treated rats J Cereb Blood Flow Metab 2008;28:1440-1448.
    [19]Judith D, Zachary P, Katherine L et al. Microstructural Status of Ipsilesional and ContralesionalCorticospinal Tract Correlates with Motor Skill in Chronic Stroke Patients[J].Hum Brain Mapp,2009,30(11):3461-3474.
    [20]Lian L, PhDl, Quan J, Guangliang D. MRI identification of white matter reorganization enhanced by erythropoietin treatment in a rat model of focal ischemia[J]. Stroke.2009 March; 40(3):936-941.
    [1]Joshua S, Robert C, Erbil A. Quantitative Diffusion-tensor Anisotropy Brain MR Imaging: Normative Human Data and Anatomic Analysis[J].Radiology,1999;21(3):770-784.
    [2]Kaori F,Masafumi H,Masako M et al. Regional changes of farctional anisotropy with normal aging using statistical parametric mapping(SPM) [J].The Journal of Medical Investigation, 2005,52(8):186-190.
    [3]David JW,ahmed TT,Christopher AC, etal. Diffusion tensor imaging can detect and quantify corticospinal tract degeneration after stroke[J]. J Neurol Neurosurg Psychiatry, 2000,69:269-272.
    [4]Pratik M,Mark M,Robert C et al. Differences between GrayMatter and White Matter Water Diffusion in Stroke:Diffusion-Tensor MR Imaging in 12 Patients[J]. Radiology, 2000,215(1):211-220.
    [5]梁志坚.脑梗死后远隔部位继发性损害的影像学诊断及其临床意义[J],国际脑血管病杂志,2008,16(4):293-295.
    [6]Mark VW, Taub E, Perkins C, et al.Poststroke Cerebral Peduncular Atrophy Correlates with a Measure of Corticospinal Tract Injury in the Cerebral Hemisphere[J]. Am J Neuroradiol, 2008,29:354-358.
    [7]张卫东,.梁碧玲.叶瑞心等.年龄对正常成人脑弥散特性影响的初步研究[J].中国医学影像学杂志,2005,13(5):336-338.
    [8]Helenius J,Sainne L,perkio J,et al. Diffusion-Weighted MR imaging in normal human brain in various age groups[J].AJNR,2002,23(2):194-199.
    [9]Chun T,Filippi C,Zimmennan R,et al.Diffusion changes in the aging human brain[J].AJNR,2000,21(6):1078-1083.,
    [10]张向前,陆兵勋,刘振华等.腔隙性脑梗死形似正常区的白质损害与超敏C 反应蛋白的关系[J].中华神经医学杂志,2009,8(4):380-384.
    [11]钟维佳,赵建农,谢微波等.脑自质稀疏症的MR弥散张量成像研究[J].重庆医科大学学报,2008,33(2):198-202
    [12]Sullivan M, Morris RG, Huckstep B, et al. Diffusion tensor MRI correlates with executive dysfunction in patients with ischaemic leukoaraiosis[J]. J Neurol Neurosurg Psychiatry,2004,75:441-447.
    [13]梁志坚,曾进胜.脑梗死远隔区继发性损害的弥散张量成像[J].国外医学脑血管疾病分册,2005,13:510-512.
    [14]Lee JS, Han MK, Kim SH, et al. Fiber tracking by diffusion tensor imaging in corticospinal tract stroke:Topographical correlation with clinical symptoms[J]. Neuroimage,2005, 26:771-776.
    [15]Kuhn MJ, Mikulis DJ, Ayoub DM et al Wallerian degeneration after cerebral infarction:evaluation with sequential MR imaging[J]. Radiology,1989,172:179-182.
    [16]王强.崔利华.张通.脑卒中后Wallerian变性和康复预后相关性研究进展[J].中国康复理论与实践,2007,11(13):1036-1038
    [17]Werring DJ, Toosy AT, Clark CA, et al. Diffusion tensor imaging can detect and quantify corticospinal tract degeneration after stroke[J]. J Neurol Neumsurg Psychiatry,2000,69(2):269.
    [18]Pierpaoli C, Bamett A, Pajevic S, et al. Water diffusion changes in Wallerian degeneration and their dependence on white matter architect- ture[J]. Neuroimage,2001,13(6 Pt 1): 1174.
    [19]Thomalla G,Glauche V,Koch MA et al.Diffusion tensor imaging detects early Wallerian degeneration of the pyramidal tract after ischemic stroke[J].Neuroimage,2004;22:1767-1774
    [20]Thomalla QGlauche V,Weiller C et al.Time course of wallerian degeneration after ischaemic stroke revealed by diffusion tensor imaging[J].. Neurol Neurosurg Psychiatry,2005,76:266-268.
    [21]曾庆师.正常人成年脑体积随年龄变化的磁共振成像定量分析[J].中国医学科学院院报,2006,28(6):795-798
    [22]Gurol ME,Irizarry MC, Smith EE, et al. Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy[J]. Neurology,2006,66:23-29.
    [23].Inoue Y, Matsumura Y, Fukuda T, et al.MRimaging of wallerian degeneration in the brain stem:temporal relationships[J].. AJNR Am J Neuroradiol,1990;11:897-902.
    [24]Hurwitz TA, Mandat T, Forster B, et al. Tract identification by novel MRI signal changes following stereotactic anterior capsulotomy[J].. Stereotact Funct Neurosurg,2006,84:228-35.
    [25]Giroud M, Fayolle H, Martin D, et al. Late thalamic atrophy in infarction of the middle cerebral artery territory in neonates. A prospective clinical and radiological study in four children[J].. Childs Nerv Sys,1995,11:133-36.
    [26]Kraemer M, Schormann T, Hagemann G, et al. Delayed shrinkage of the brain after ischemic stroke:preliminary observations with voxel-guidedmorphometry[J].. J Neuroimaging,2004,14:265-72.
    [1]Barker A,Jalimous R,Freeston I,et al.Non-invasive magnetic stimulation of human motor cortex[J]..Lancet,1985,1(8437):1106-1107.
    [2]Ueno S. functional mapping of the human motor cortex obtained by focal and vectorial magnetic stimulation of the brain[J]..IEEEE transaction on magnetics,1990,26:1539
    [3]Abbruzzese G, Morena M. Motor evoked potentials in laeunar syndromes[J]. Electroencephalogr Clin Neurophysiol,1991,81:202-208.
    [4]Chokroverty S,Picone M,chocroverty M.Percutaneous magnetic coilstimulation of human cervical vertebral column:site of stimulation and clinical application[J].. "Eleetroencephalegr Clin Neurephysiol,1991,81:359-365.
    [5]Cruz—Martinez A, Munoz J, Palacios F. The muscle inhibitory pe—riod by transcranial magnetic stimulation:study in stroke patients[J]. EMG Clin Neurophysiol,1998,38:189-192.
    [6]Hendricks HT, Hageman G, Van—Limbeeek J. Prediction of recovery from upper extremity paralysis after stroke by measuring evoked potentials [J]. Scand J Rehabil Med,1997,29:155-159.
    [7]Roger Q, Cracco RQ. Evaluation of conduction in central motor pathways: techniques pathophysiology and clinical interpretation[J]. Neurosurg,1987,20: 199-203.
    [8]Pascual-Leone A,Cohen LG,Shotland Li,et al.No evidence of hearing loss in humans due to transcranial magnetic stimulation[J].Neurology,1992,42(3 Pt1):647-651.
    [9]EseuderodV, Sancho J. Bau. tista D. Prognostic value of motor evoked potential obtained by transcranial magnetic brain stimulation in motor function recovery in patients with acute lschemie stroke[J].. Stroke,1998,29(9):1854.
    [10]吴克芬,杨建伟,李泽兵.经颅磁刺激对脑卒中患者运动功能的预测价值[J].国外医学·物理医学与康复学分册,2003,23(1):33-34.
    [11]张向东,刘恒方,杨清成.脑梗死后运动功能的可塑性研究[J]..中国实用神经疾病杂志.2006,11(9):6-8.
    [2]黄琚.运动诱发电位[J]..国外医学·物理医学与康复学分册[J]..2005,25(2)56-58.
    [13]Pennisi G, Rapisarda G, Bella R, et al. Absence of response to early transcranial magnetic stimulation in ischemic stroke patients:prognostic value for hand motor recovery[J].. Stroke,1999,30(12):2666-2670.
    [14]王强.崔利华.张通.脑卒中后Wallerian变性和康复预后相关性研究进展[J]..中国康复理论与实践,2007;11(13):1036-1038.
    [15]邢岩.经颅磁刺激技术在缺血性脑血管病中的研究进展[J].,国际神经病学神经外科学杂志,2007,34(1):64-67.
    [1]Barker A,Jalimous R,Freeston I,et al.Non-invasive magnetic stimulation of human motor cortex[J]..Lancet,1985,1 (8437):1106-1107.
    [2]Ueno S. functional mapping of the human motor cortex obtained by focal and vectorial magnetic stimulation of the brain[J].IEEEE transaction on magnetics,1990,26:1539.
    [3]Pascual-Leone A,Cohen LG,Shotland Li,et al.No evidence of hearing loss in humans due to transcranial magnetic stimulation [J].Neurology,1992,42(3 Ptl):647-651.
    [4]Chokroverty S, Hening W, Wright D,et al.Magnetic brain stimulation:safety studies[J]..electroenphaglogr Clin Neurophysiol,1995,97(1):36-42.
    [5]郑安洁,程焱.重复经颅磁刺激在脑梗死后运动康复中的应用[J].国际脑血管疾病杂志,2007,15(10):749-752.
    [6]陈炜.经颅短串电刺激运动诱发电位的临床应用[J]..中国临床神经病学杂志,2003,11(2):215-217.
    [7]余锋,赵合庆,孙永安.经颅磁刺激对脑缺血一再灌注大鼠急性期脑内单胺类神经递质含量的影响[J]..中国脑血管疾病杂志,4(2):76-80.
    [8]孙永安赵合庆.经颅磁刺激与脑梗死[J].国外医学脑血管疾病分册,2002,10(6):432-434
    [9]Speer AM, KhnbreⅡ TA, WasseHnann EM, et al Opposite effects of high and low frequency rTMS on regional brain activity in depressed patients [J]. Biol Psychiatry, 2000,48(12):1133-1141.
    [10]郭风劲,李新志,许涛,等,磁刺激对脊髓神经组织损伤的早期保护作用[J]中国康复,2001,16:4-6
    [11]Ward N, Brown M, Thompson A, et al. Neural correlates of motor recovery after stroke:a longitudinal fMRI study[J]..Brain,2003,126(13):2476-2496.
    [12]Pal K, Hanajima R, Gunraj CA, et al. Effect of low-frequency repetitive transcmnial magnetic stimulation on interhemispheric inhibition[J].. J Neurophysiol, 2005,94(10):1668.1675.
    [13]Kobayashi M, Hutchinson S, Theoret H, et al. RepetitiveTMS of the motor cortex improves ipsilateral sequential simple finger movements[J].. Neurology,2004, 62(2):91-98.
    [14]Di Lazzaw V, Dileone M, Profice C, et al. Direct demonstration that repetitive transcranial magnetic stimuhfion can enhance corticospinal excitability in stroke[J].Stroke,2006,37(8):2850-2853.
    [15]Huang YZ, Edwards MJ, Rounis E, et ul. Thets burst stimulation of the human motor cortex [J]. Neuron,2005,45(4):201.206.
    [16]Martin P, Naeser M. Tranacranial magnetic stimulation a complementary treatment for aphasia[J]. Semin Speech Lang,2004,25(2):181-191.
    [17]Fregni F, Boggio P. A Sham-Controlled Trial of a 5. Day Course of Repetitive Tranacranial Magnetic Stimulation of the Unaffected Hemisphere in Stroke Patients[J]. Stroke,2006,37(12):2108-2115.
    [18]Khedr E, Ahmed M, Fathy N, et al. Therapeutic trial of repetitive transcranial magnetic stimulation after acute ischemic stroke[J]. Neurology,2005,65(3):353-354.
    [19]齐力.电刺激小脑顶核改善缺血性脑损害的研究进展[J].国外医学脑血管疾病分册,1996,4(1):33-35.
    [20]Andoh J. Martinot JL. Interhemispheric compensation:a hypothesis of TMS-induced effects on language-related areas[J]. Eur Psychiatry,2008,23(4): 281-288.
    [21]庄立.重复经颅磁刺激改善缺血性脑卒中运动功能的作用机制[J].中国神经免疫学和神经病学杂志.2009,16(3):213-216
    [22]Michael A. Leonardo G. Contribution of transcranial magnetic stimulation to the understanding of mechanisms of functional recovery after stroke[J]. Neurorehabil Neural Repair.2010,24(2):125-135.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700