扩散张量成像辨别脑白质高信号异质性的研究

目的 探讨使用扩散张量成像(DTI)辨别不同类型的脑白质高信号(WMH).方法 对73例WMH患者和18例健康志愿者(对照组)行DTI检查,比较额叶、枕叶、顶叶脑室旁和额顶叶半卵圆中心正常脑白质和WMH的各DTI参数.结果 不同部位DTI参数的变化幅度有差异,与正常脑白质相比,额叶Fazekas 1级WMH的部分各向异...     

基于扩散张量成像的面肌痉挛患者脑白质异常分析

目的 探讨面肌痉挛(H FS)患者全脑白质结构的异常以及与临床特征的相关性.方法 26例H FS患者(患者组)和29例健康志愿者(对照组)纳入本研究.应用基于纤维束的空间统计方法(TBSS)分析患者组与对照组各项扩散张量成像(DTI)参数的差异,并与患者的面部肌肉痉挛程度进行相关分析.结果 与对照组相比,患者组胼胝体膝...     

扩散张量成像技术及在脑白质病变中的应用

扩散张量成像(DTI)是一种崭新的MRI技术,它对组织内水的扩散在三维空间进行考察,比常规扩散加权成像能更好地反映生物组织扩散的各向异性.叙述了DTI的成像技术、数据处理及其衍生的量化信息、DTI对一些脑白质病变检查和评价的作用.     

扩散张量成像技术及在脑白质病变中的应用

扩散张量成像(DTI)是一种崭新的MRI技术，它对组织内水的扩散在三维空间进行考察。比常规扩散加权成像能更好地反映生物组织扩散的各向异性。叙述了DTI的成像技术、数据处理及其衍生的量化信息、DTI对一些脑白质病变检查和评价的作用。     

脑白质疏松的扩散张量成像(DTI)研究

目的 应用扩散张量成像（DTI）检查脑白质疏松（LA）病灶的平均扩散系数（DCavg）、各向异性（FA）值与LA严重程度的关系,探讨常规MBI检查正常的脑白质微结构在DTI中的变化及与认知功能的关系。资料与方法 对55例LA患者和22名健康老年人行DTI检查,测量LA病灶和正常白质区域的DCavg、FA值。结果 LA程度越严重,DCavg值越高,呈正相关;FA值越低,呈负相关。神经心理学测试（简易智能精神状态量表,MMSE）与LA患者的正常脑白质区域的DCavg、FA值明显相关,尤其是前角白质、半卵圆中心的正常脑白质。结论 DTI检查LA,其DCavg、FA值显示出特征性的改变,DTI能够发现常规MRI检查正常的脑白质微结构改变,且这种改变与认知功能相关。     

创伤性脑白质损伤的扩散张量成像研究

目的:评价扩散张量成像(DTI)在创伤性脑白质损伤(WMI)中的应用价值。方法:16例创伤性脑外伤后经临床诊断有WMI的患者通过Philips 1.5TIntera Achieva MR扫描仪行常规MRI和DTI。后处理获得部分各向异性指数(FA)、表观弥散系数(ADC)和纤维示踪成像三维图。根据T2WI及T2快速场回波图像,分别于WMI区域、同侧同名或对侧同名纤维束正常区域取感兴趣区,测量FA值和ADC值并进行比较。结果:脑外伤患者损伤脑白质中挫伤和出血、仅挫伤和仅出血区域三者之间的FA值(F=0.68,P>0.05)和ADC值(F=0.53,P>0.05)均未见明显不同。除仅出血区域的ADC值与对照区域相比差异无统计学意义(t=1.36,P>0.05),挫伤和出血(t=9.72,P<0.05)、仅挫伤(t=8.28,P<0.05)和仅出血(t=5.44,P<0.05)区域的FA值较正常对照区域明显降低,挫伤和出血(t=4.71,P<0.05)、仅挫伤(t=4.81,P<0.05)的ADC值较正常对照明显增高,纤维示踪成像显示损伤区域脑白质较正常区域稀疏、分离、缺失。结论:DTI技术能够显示患者WMI区域的异常改变,但ADC值对出血的判断有局限性。     

扩散张量成像对正常儿童脑白质结构的初步探讨--彩色张量图的应用

目的　分析正常儿童的脑彩色张量图表现 ,探讨扩散张量成像对评价儿童脑发育的价值。方法　对 89名正常儿童 (年龄 2d～ 18岁 )行头部扩散张量成像 ,分析不同年龄段、不同白质纤维束的显示情况并总结规律。结果　不同年龄段正常儿童的彩色扩散图表现不同 ,随年龄增长 ,可显示的白质纤维束增多 ,边界逐渐清晰 ,5岁以后表现接近于成人。结论　彩色张量图适用于直观评价儿童脑白质的发育情况 ,优于常规磁共振成像     

首发抑郁症患者脑白质微结构异常的扩散张量成像研究

目的 应用磁共振扩散张量成像(DTI)技术研究首次发作抑郁症(MDD)患者脑白质微结构改变.资料与方法 对22例首次发作MDD患者和30例性别、年龄和受教育程度相匹配的正常对照者进行全脑DTI扫描.应用基于体素的形态学分析法比较两组受检者的各向异性分数(FA),并分析MDD患者脑白质微结构改变与MDD病程及严重程度的相...     

正常老年脑及脑白质疏松症的MR扩散张量成像

介绍了MR扩散张量成像在正常老年脑及脑白质疏松症中的应用,以及其在活体评价脑功能改变的状况.     

脑磁共振扩散张量成像术及其进展

分子扩散是一个三维空间的运动,在某些组织如脑白质中的运动是各向异性的.磁共振脑扩散张量可分辨出分子扩散运动方向上的差异,因而可显示组织扩散各向异性的细微异常.就磁共振扩散张量成像的基本原理、技术特点及成像可视化技术的基本概念予以综述.     

Diffusion Tensor Imaging Mapping of Brain White Matter Pathology in Mitochondrial Optic Neuropathies

BACKGROUND AND PURPOSE:Brain white matter is frequently affected in mitochondrial diseases; optic atrophy gene 1-autosomal dominant optic atrophy and Leber hereditary optic neuropathy are the most frequent mitochondrial monosymptomatic optic neuropathies. In this observational study, brain white matter microstructure was characterized by DTI in patients with optic atrophy gene 1-autosomal dominant optic atrophy and Leber hereditary optic neuropathy, in relation to clinical and genetic features.MATERIALS AND METHODS:Nineteen patients with optic atrophy gene 1-autosomal dominant optic atrophy and 17 with Leber hereditary optic neuropathy older than 18 years of age, all genetically diagnosed, and 19 healthy volunteers underwent DTI by using a 1.5T MR imaging scanner and neurologic and ophthalmologic assessments. Brain white matter DTI metrics were calculated for all participants, and, in patients, their correlations with genetics and clinical findings were calculated.RESULTS:Compared with controls, patients with optic atrophy gene 1-autosomal dominant optic atrophy had an increased mean diffusivity in 29.2% of voxels analyzed within major white matter tracts distributed throughout the brain, while fractional anisotropy was reduced in 30.3% of voxels. For patients with Leber hereditary optic neuropathy, the proportion of altered voxels was only 0.5% and 5.5%, respectively, of which half was found within the optic radiation and 3.5%, in the smaller acoustic radiation. In almost all regions, fractional anisotropy diminished with age in patients with optic atrophy gene 1-autosomal dominant optic atrophy and correlated with average retinal nerve fiber layer thickness in several areas. Mean diffusivity increased in those with a missense mutation. Patients with Leber hereditary optic neuropathy taking idebenone had slightly milder changes.CONCLUSIONS:Patients with Leber hereditary optic neuropathy had preferential involvement of the optic and acoustic radiations, consistent with trans-synaptic degeneration, whereas patients with optic atrophy gene 1-autosomal dominant optic atrophy presented with widespread involvement suggestive of a multisystemic, possibly a congenital/developmental, disorder. White matter changes in Leber hereditary optic neuropathy and optic atrophy gene 1-autosomal dominant optic atrophy may be exploitable as biomarkers.

Mutations in optic atrophy gene 1 are the main cause of autosomal dominant optic atrophy (DOA) (Online Mendelian Inheritance in Man 605290).^1,2 DOA is characterized clinically by insidiously progressive visual loss in childhood, centrocecal scotoma, dyschromatopsia, and temporal or diffuse pallor of the optic discs, due to selective loss of retinal ganglion cells leading to atrophy of the optic nerve.^1,2 Similarly, Leber hereditary optic neuropathy (LHON) (Online Mendelian Inheritance in Man 535000) is characterized by subacute loss of central vision, dyschromatopsia, and optic atrophy due to maternally inherited point mutations in mitochondrial DNA that affect respiratory complex I.^1,2DOA and LHON represent the so-called nonsyndromic mitochondrial optic neuropathies, characterized by optic nerve atrophy as the only or at least prevalent pathologic feature with an early and preferential involvement of the small fibers in the papillomacular bundle.^3,4 Recent MR imaging studies by using voxel-based morphometry,⁵ DWI,⁶ and DTI⁷ have also indicated abnormalities of the optic radiation in patients with LHON, confirmed by postmortem investigation,⁶ suggesting a trans-synaptic degeneration. A similar secondary involvement of the retrogeniculate visual pathway could also be hypothesized in patients with DOA. Furthermore, given that the optic atrophy gene 1 (OPA1) is highly expressed in the retina but also in the brain^1,2,8 and that a subgroup of patients with specific OPA1 mutations have a multisystem neurologic disorder,⁹ it is reasonable to also hypothesize a subclinical extravisual brain involvement in patients with OPA1-DOA.The aim of the present study was to investigate the brain white matter of patients with OPA1-DOA compared with those with LHON and healthy controls, by using a voxelwise analysis of DTI, which can disclose abnormal water diffusivity in brain areas where atrophy and/or gliosis occur,¹⁰ to look for subtle structural alterations.     

磁共振弥散张量纤维束成像在评估脑肿瘤白质纤维束变化中的价值

目的 探讨磁共振弥散张量纤维束成像(DTT)在评估脑肿瘤中脑白质纤维束变化的价值.方法 运用DTT技术分别评价胶母细胞瘤、脑膜瘤、间变性星形细胞瘤脑白质纤维束的变化.结果 脑肿瘤旁脑白质纤维束在DTT可有以下3种表现:(1)中断,(2)移位,(3)浸润.其中,在胶母细胞瘤中,可见脑白质纤维束中断, 其终止纤维可通过胼胝体;在脑膜瘤中,可见肿瘤压迫引起的脑白质纤维移位以及残存、被分离的纤维束;在间变性星形细胞瘤中,DTT表现为肿瘤原发部位脑白质纤维束中断以及肿瘤对轴突的浸润.结论 DTT的异常表现与肿瘤临床病理特征相关.     

Brain White Matter Involvement in Hereditary Spastic Paraplegias: Analysis with Multiple Diffusion Tensor Indices

BACKGROUND AND PURPOSE:The hereditary spastic paraplegias are a group of genetically heterogeneous neurodegenerative disorders, characterized by progressive spasticity and weakness of the lower limbs. Although conventional brain MR imaging findings are normal in patients with pure hereditary spastic paraplegia, microstructural alteration in the cerebral WM can be revealed with DTI. Concomitant investigation of multiple intrinsic diffusivities may shed light on the neurobiologic substrate of the WM degeneration pattern in patients with pure hereditary spastic paraplegia across the whole brain.MATERIALS AND METHODS:Tract-based spatial statistics analysis was performed to compare fractional anisotropy and mean, axial, and radial diffusivities of the WM skeleton in a group of 12 patients with pure hereditary spastic paraplegia and 12 healthy volunteers. Data were analyzed counting age and sex as nuisance covariates. The threshold-free cluster-enhancement option was applied, and the family-wise error rate was controlled by using permutation tests for nonparametric statistics.RESULTS:In pure hereditary spastic paraplegia, group widespread fractional anisotropy decreases and radial diffusivity and mean diffusivity increases (P < .05, corrected) were found. No voxelwise difference was observed for the axial diffusivity map. Percentage of voxels within the WM skeleton that passed the significance threshold were 51%, 41.6%, and 11.9%, respectively, for radial diffusivity, fractional anisotropy, and mean diffusivity clusters. An anteroposterior pattern with preferential decrease of fractional anisotropy in the frontal circuitry was detected.CONCLUSIONS:In patients with pure hereditary spastic paraplegia, alterations in multiple DTI indices were found. Radial diffusivity seems more sensitive to hereditary spastic paraplegia–related WM pathology and, in line with the lack of axial diffusivity changes, might indicate a widespread loss of myelin integrity. A decrease of fractional anisotropy alone in the frontal circuitry may reflect subtle disruption of the frontal connections.

The hereditary spastic paraplegias (HSPs), also called familial spastic paraparesis or Strümpell-Lorrain disease, represent a genetically and clinically heterogeneous group of neurodegenerative disorders.¹ The main clinical feature is progressive spasticity due to slowly progressing “dying back” axonal degeneration, which is maximal in the terminal portions of the longest descending and ascending tracts.² On the basis of clinical symptoms, HSPs are classified into pure or uncomplicated, in which the spastic paraplegia is the major clinical manifestation; and complex or complicated forms, presenting with additional neurologic signs, such as intellectual disability or cognitive decline, deafness, cerebellar ataxia, epilepsy, dysarthria, peripheral neuropathy, optic atrophy, and visual dysfunction.³ Autosomal dominant, autosomal recessive, or X-linked inheritance is associated with multiple genes or loci and leads to genetic heterogeneity of this disorder. The HSP loci are designated as spastic paraplegia loci and are numbered 1–56 according to their discovery.⁴ There is scarce evidence about the epidemiology of HSP, though its prevalence is estimated at 1.27:100,000 population in Europe.⁵Findings of conventional MR imaging of the brain are usually normal in pure hereditary spastic paraplegia (pHSP). In contrast, nonspecific findings such as cortical atrophy and subcortical and periventricular WM alterations are present in complicated HSP.⁶ Distinct MR imaging findings may accompany complicated HSP; for instance, a common form of autosomal recessive HSP with SPG11 mutation (linked to the 15q13-q15 chromosome) is frequently associated with a thin corpus callosum.⁷ Optic nerve and cerebellar atrophy may be revealed when visual symptoms and cerebellar ataxia are present.⁸DTI is an efficient technique used to characterize the in vivo microstructural organization of the WM.⁹ The common DTI indices are fractional anisotropy (FA) (sensitive to microstructural changes and associated with the presence of oriented structures in tissue) and mean diffusivity (MD) (characterizes mean-square displacement of molecules and the overall presence of obstacles to diffusion).¹⁰ Other indices, axial diffusivity (AD) and radial diffusivity (RD), offer suggestive elements to differentiate axonal injury and demyelination.¹¹ To extend our knowledge of the neurobiologic basis of WM pathology, using multiple diffusivity matrices (FA, MD, RD, and AD) is recommended.¹²The present study was set up to investigate WM alterations across the whole brain in a group of patients with pHSP with SPG4, SPG5, SPG3a, and SPG10 mutations, applying tract-based spatial statistics (TBSS) analysis with multiple DTI indices.     

磁共振DTI及DTT在脑梗死白质纤维束损伤中的应用

目的：探讨MR扩散张量成像（DTI）及扩散张量纤维束成像（DTT）技术对不同时期脑梗死白质损伤的诊断价值,并观察白质纤维束的受损情况,为脑梗死后患侧肌力恢复治疗提供影像学依据。方法：53例脑梗死患者按不同发病时期分为4组,行常规MRI及DTI检查,对比测量梗死侧与健侧相应部位脑白质的各向异性系数（FA）值,并观察梗死灶白质纤维柬的改变,按照皮质脊髓束（CST）移位、连续性及破坏程度在DTT图像上的表现分为3级。结果：超急性期梗死侧FA值（0．35±0．04）与健侧（0．37±0．06）比较差异无统计学意义（P〉0．05）,急性期、亚急性期和慢性期梗死侧FA值分别为0．17±0．07、0．14±0．06和0．09±0．05,分别低于健侧相应部位的FA值（分别为0．39±0．08、0．36±0．08和0．33±0．06）,差异均有显著性意义（P〈0．05）。3组DTT分级比较差异无统计学意义（P〉0．05）,患侧肌力改变与皮质脊髓束损伤程度呈正相关（rs=0．76,P〈0．05）,皮质脊髓束损伤程度可以通过重建的扩散张量纤维束成像显示。结论：DTI及DTT技术能较好的评价不同时期脑梗死白质纤维束的损伤程度,对指导临床诊断和帮助判断预后有重要价值。     

基于扩散张量成像利用一阶有限元方法计算脑白质各向异性电导率对脑电位分布的影响

目的 研究脑白质各向异性电导率对头皮电位分布的影响.方法 把由扩散张量成像得到的水分子扩散张量采用体积约束规则计算出白质组织的电导率张量,并根据成像的空间信息建立了包括头皮、颅骨、灰质、脑脊液及白质5种组织的真实头的有限元模型.基于此模型,推导了各向异性电导率脑电正问题的一阶有限元数值算法.最后,采用电流偶极子模型计算头皮电位分布.结果 脑白质各向异性电导率对头皮电位分布有一定的影响,径切比越大,影响越大;左右分布偶极子比上下分布的影响要大.结论 脑电研究中,白质电导率的各向异性为一不可忽略的因素.     

Diffusion Tensor Imaging of White Matter in Children Born from Preeclamptic Gestations

BACKGROUND AND PURPOSE:Individuals born from pregnancies complicated by preeclampsia have an elevated risk for cognitive impairment. Deviations in maternal plasma angiokines occur for prolonged intervals before clinical signs of preeclampsia. We hypothesized that fetal brain vascular and nervous tissue development become deviated during maternal progression toward preeclampsia and that such deviations would be detectable by MR imaging.MATERIALS AND METHODS:In this pilot study, 10 matched (gestational and current ages) pairs (5 boys/5 girls, 7–10 years of age) from preeclampsia or control pregnancies were examined by using diffusion tensor MR imaging. An unbiased voxel-based analysis was conducted on fractional anisotropy and mean diffusivity parametric maps. Six brain ROIs were identified for subsequent analysis by tractography (middle occipital gyrus, caudate nucleus and precuneus, cerebellum, superior longitudinal fasciculus, and cingulate gyrus).RESULTS:Statistical differences were present between groups for fractional anisotropy in the caudate nucleus (offspring from preeclamptic gestation > controls), volume of the tract for the superior longitudinal fasciculus (offspring from preeclamptic gestation > controls) and the caudate nucleus (offspring from preeclamptic gestation > controls), and for parallel diffusivity of the cingulate gyrus (offspring from preeclamptic gestation > controls).CONCLUSIONS:These novel preliminary results along with previous results from the same children that identified altered cerebral vessel calibers and increased regional brain volumes justify fully powered MR imaging studies to address the impact of preeclampsia on human fetal brain development.

Hypertensive disorders during human pregnancy include acute-onset emergency preeclampsia (PE), seen at a frequency of 2%–8% of all gestations.¹ PE is a systemic vascular inflammatory syndrome occurring between midpregnancy and term and is the leading cause of maternal and fetal morbidity and mortality. Up to 12% of annual maternal deaths² and up to 25% of annual fetal and neonatal deaths globally³ are PE-associated. Leading hypotheses addressing the pathophysiology of PE focus on progressive deficits in uteroplacental angiogenesis and maternal vascular remodeling well before the onset of clinical signs, due to an imbalance in angiokines and soluble angiokine receptors, which are predominantly products of the placenta.⁴A recent systematic review of the impact of maternal hypertension (all forms) during pregnancy on offspring addressed outcomes after 6 months of life. The review identified cardiovascular, immune, metabolic, and behavioral/neurologic effects on individuals born from preeclamptic mothers (PE-F1s). For PE-F1s, lower cognitive function was the prominent, reliable association.⁵ The deficits in cognitive functions reported for PE-F1s^5–7 include lower intelligence quotient scores,^8,9 reduced verbal and nonverbal abilities,^10,11 and reduced arithmetic reasoning.^12,13Recently, we conducted a pilot study to determine whether clinical cognitive function test outcomes and brain MR imaging findings differed between PE-F1s and typical 7- to 10-year-old children.¹⁴ The hypothesis driving this research posits that the progressive dysregulation of angiokines that is clinically associated with maternal PE development reflects conditions occurring not only in placental but also in all fetal tissues and impacts fetal cerebrovascular development. This hypothesis¹⁵ predicts that brain anatomy and function differ between PE-F1s and children born from normotensive mothers due to the use of common molecular pathways during vascular and neuronal cell differentiation (vascular endothelial growth factor pathways) and to the importance of cerebral blood flow for anatomic and functional brain development. Our pilot study suggested specific deficits in cognitive testing and in eye-movement control.¹⁶ Initial volumetric analyses of brain anatomic regions by using high-resolution T1-weighted MR imaging datasets identified 5 regions of anatomic enlargement in PE-F1s (cerebellum, temporal lobe, left amygdala, right amygdala, and brain stem). In addition, reduced vascular radii were identified from time-of-flight MR angiography datasets in the occipital and parietal lobes.¹⁴ These preliminary results were the first reported MR imaging/MRA findings in PE-F1s of any age group.The aim of the current study was to determine whether microstructural properties, including myelination patterns and white matter connectivity analyzed by diffusion tensor MR imaging, differ between PE-F1s and matched typical children. A further goal was to assess whether DTI findings overlapped the previously identified anatomic or vascular deviations in these children.¹⁴     

复发好转型多发性硬化表现正常脑白质DTI研究

目的:利用扩散张量成像(DTI)直方图分析,明确复发好转型多发性硬化(RRMS)患者表现正常脑白质(NAWM)的异常改变及DTI直方图指标与扩展残疾状态(EDSS)评分的相关性。方法:对29例RRMS患者和35例健康志愿者行常规MRI和DTI检查,分割提取NAWM后,绘制出NAWM的平均扩散率(MD)和部分各向异性(FA)直方图,并对其进行分析。结果:与健康志愿者比较,RRMS患者NAWM平均MD直方图右移、峰高降低;平均FA直方图左移、峰高增高。RRMS患者NAWM的平均MD、MD直方图峰位置和FA直方图峰高明显高于健康志愿者(P<0.001),而MD直方图峰高和平均FA明显低于健康志愿者(P<0.001)。在RRMS患者,所有NAWM的MD和FA直方图指标与EDSS评分均无相关性。结论:RRMS患者NAWM内存在明显扩散异常。     

Effect of Increasing Diffusion Gradient Direction Number on Diffusion Tensor Imaging Fiber Tracking in the Human Brain

Objective

To assess the effects of varying the number of diffusion gradient directions (NDGDs) on diffusion tensor fiber tracking (FT) in human brain white matter using tract characteristics.

Materials and Methods

Twelve normal volunteers underwent diffusion tensor imaging (DTI) scanning with NDGDs of 6, 11, 15, 21, and 31 orientations. Three fiber tract groups, including the splenium of the corpus callosum (CC), the entire CC, and the full brain tract, were reconstructed by deterministic DTI-FT. Tract architecture was first qualitatively evaluated by visual observation. Six quantitative tract characteristics, including the number of fibers (NF), average length (AL), fractional anisotropy (FA), relative anisotropy (RA), mean diffusivity (MD), and volume ratio (VR) were measured for the splenium of the CC at the tract branch level, for the entire CC at tract level, and for the full brain tract at the whole brain level. Visual results and those of NF, AL, FA, RA, MD, and VR were compared among the five different NDGDs.

Results

The DTI-FT with NDGD of 11, 15, 21, and 31 orientations gave better tracking results compared with NDGD of 6 after the visual evaluation. NF, FA, RA, MD, and VR values with NDGD of six were significantly greater (smallest p = 0.001 to largest p = 0.042) than those with four other NDGDs (11, 15, 21, or 31 orientations), whereas AL measured with NDGD of six was significantly smaller (smallest p = 0.001 to largest p = 0.041) than with four other NDGDs (11, 15, 21, or 31 orientations). No significant differences were observed in the results among the four NDGD groups of 11, 15, 21, and 31 directions (smallest p = 0.059 to largest p = 1.000).

Conclusion

The main fiber tracts were detected with NDGD of six orientations; however, the use of larger NDGD (≥ 11 orientations) could provide improved tract characteristics at the expense of longer scanning time.     

颞叶癫痫患者的颞叶以外白质MR扩散张量成像研究

目的 应用MR扩散张量成像(DTI)探讨颞叶癫痫(TLE)患者的颞叶以外白质是否存在隐匿性损伤,并研究这些白质结构的DTI参数值与患者初次发病年龄及病程长短的相关性.资料与方法 对临床确诊的42例发作间期TLE患者和32名健康志愿者行常规MRI和DTI检查,定量测量胼胝体膝部、体部、压部、内囊前肢、后肢及外囊的平均扩散系数(Dcavg)和部分各向异性(FA)值并进行统计学分析.结果 TLE患者胼胝体压部、内囊后肢及外囊的Dcavg值显著高于正常人(P<0.01),胼胝体膝部、压部、内囊前肢及外囊的FA值显著低于正常人(P<0.05).TLE患者内囊后肢Dcavg值与病程长短呈正相关.结论 TLE患者的颞叶以外白质存在隐匿性损伤,内囊后肢的损伤程度与病程长短有关.     

多发性硬化的正常表现脑白质的DTI定量

目的：应用磁共振弥散张量成像（DTI）技术，定量研究多发性硬化（MS）患者在常规磁共振上表现正常的脑白质（NAWM），以及探讨其相关的微观病理改变。材料和方法：采用3．0T磁共振仪，对34例Ms患者和25例性别年龄相匹配的正常志愿者均进行DTI检查。分别测量MS组和对照组的9个不同部位脑白质的平均弥散率（MD）和部分各向异性指数（FA值），这9个部位包括胼胝体膝部、体部、压部、内囊后肢、侧脑室旁白质、额叶白质、顶叶白质、枕叶白质以及小脑中脚。比较两组NAWM之间的MD和FA值是否存在差异。结果：MS组的NAWM的MD值均高于对照组（P〈0．05），以胼胝体体部、内囊、侧脑室旁及额叶白质、顶叶白质、枕叶白质更为显著（P〈0．01）；MS组的FA值与对照组比较，胼胝体体部、顶叶白质、额叶白质、枕叶白质及内囊、侧脑室旁发现明显降低（P〈0．05），以后4个部位更为显著（P〈0．01），而胼胝体膝部、压部和小脑结合臂有降低趋势，但无统计学意义。结论：应用DTI定量研究可以探测到多发性硬化的NAWM所出现的微观病理改变，表现为水分子的平均弥散幅度明显升高，以幕上明显，并且胼胝体体部、内囊后肢等白质纤维明显失去正常的方向性。DTI在对白质损伤程度的量化评估中具有重要的价值。