扩散张量成像对早期帕金森病轻度认知障碍高危患者脑白质微结构改变的纵向分析

目的 探讨早期帕金森病轻度认知障碍(PD-MCI)高危患者脑白质微结构的纵向改变.方法 采用扩散张量成像(DTI)及认知量表对来自PPMI数据库的83例认知正常PD(PD-NC)患者进行4年的随访,其中26例进展为PD-MCI(NC-MCI组),57例认知保持正常(NC-stable组).采用基于纤维束示踪的空间统计分...     

早期帕金森病患者脑白质损害的扩散张量成像研究

目的:采用基于纤维束示踪的空间统计方法分析(TBSS)早期帕金森病患者扩散张量成像(DTI)数据,研究早期帕金森病患者脑白质结构损害情况及与运动症状的相关性.方法:18例早期帕金森病(PD)患者(Hoehn-Yahr 1～2级)及22例健康志愿者(对照组)行DTI扫描,采用TBSS技术对两组受试者的DTI数据进行分析,比较两组受试者脑白质纤维的部分各向异性(FA)值的差异,及其与帕金森病评估量表(UPDRS-Ⅲ)评分的相关性,测量并比较先发病侧与对侧大脑白质的FA值.结果:全脑分析显示:与正常对照组相比,PD组双侧额顶部、放射冠、胼胝体和扣带回的脑白质FA值明显减低(P＜0.05),且其范围均与UPDRS-Ⅲ评分呈负相关(r=-0.479～-0.736,P＜0.05);早期PD患者先发病侧大脑与对侧大脑比较,后放射冠、顶叶及颞叶的脑白质FA值的差异有统计学意义(P＜0.05).结论:早期PD患者即可见脑白质纤维结构的改变,大脑白质损害程度与PD患者运动症状有密切联系,PD患者脑白质损害的部位可能存在一定的顺序.     

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...     

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...     

扩散张量成像对胶质瘤分级的应用价值

胶质瘤是脑内最常见的恶性肿瘤,胶质瘤分级对其治疗方案的选择及预后判断尤为重要。扩散张量成像(DTI)是目前唯一可以在活体状态下无创性检测组织微观结构的功能成像方法。DTI对水分子运动敏感,尤其是沿着轴突纤维束分布的水分子,而胶质瘤肿瘤细胞浸润主要沿着白质神经束走行,低级别胶质瘤的神经轴扩散率为3.7%~5.3%,而高级别胶质瘤为10%~27%,因此DTI对胶质瘤的分级诊断具有重要的价值。现就近年来DTI对胶质瘤分级诊断的研究现状及研究前景等方面内容进行综述。     

脑缺血性卒中MR扩散张量成像的初步研究

目的利用磁共振扩散张量成像(DTI)及扩散张量纤维束成像(DTT)评价缺血性脑卒中所致皮质脊髓束(CST)损伤程度与运动功能的关系。方法对9例急性期大脑中动脉供血区缺血性脑卒中病人进行常规MR、DTI和DTT检查,对数据进行离线后处理,采用dTV.II软件处理,获得FA图及方向编码彩色图,并重建双侧皮质脊髓束3D纤维束图。对梗死区及健侧相应区域白质进行FA测量。采用Brunnstorm标准判断脑卒中患者患手肌力。结果在脑卒中病人梗死区FA值显著低于健侧,两侧相比差异有显著统计学意义(t=4.570,P<0.001)。病变侧皮质脊髓束表现为受压、变形、移位和中断,皮质脊髓束受累情况与肌力和运动功能的恢复有良好的相关性(rs=0.888,P<0.05)。结论CST损伤严重程度与运动功能的恢复相关,DTI和DTT对观察CST的损害程度、预测恢复程度、指导临床康复治疗具有重要的价值。     

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。     

脑梗死患者磁共振扩散张量纤维束成像的随访研究

目的应用磁共振扩散张量纤维束成像(DTT)研究梗死灶与皮质脊髓束的空间关系,并随访观察受损纤维束的功能重组与代偿情况,探讨DTT技术对预测患者运动功能转归的价值。方法选择左侧内囊周围区脑梗死患者19例,分别于发病7、30、90天进行磁共振扩散张量成像(DTI)检查,应用DTT技术进行皮质脊髓束三维重建,采用FuglMeyer量表评价患者的运动功能,分析脑梗死灶及皮质脊髓束受累程度与患者运动功能恢复的关系。结果 DTT显示19例左侧内囊周围区梗死患者,根据患侧皮质脊髓束受累情况分为3型,I型5例,皮质脊髓束位于梗死灶外,FM评分96.46±7.68;II型6例,皮质脊髓束部分位于梗死灶内,但受侵范围1/3;或受压、迂曲、推移改变,FM评分94.20±6.84;III型8例,皮质脊髓束1/3位于梗死灶内,FM评分82.37±22.14。19例患者发病7天,皮质脊髓束损伤分型与FM评分呈显著负相关(r=-0.490,P=0.033)。DTT对患者皮质脊髓束的动态观察显示,8例III型患者中4例90天皮质脊髓束显示良好,患者运动功能完全恢复;2例患者皮质脊髓束自身发生再生修复,90天后仅遗留部分运动功能障碍;2例未发现纤维再生修复,90天仍遗留严重运动功能障碍。结论 DTT能够直观显示脑梗死患者的皮质脊髓束受累程度及其动态变化,对评价其运动功能恢复提供重要的客观影像学依据。     

磁共振扩散张量成像在判断脑梗死预后中的初步研究

目的 用磁共振扩散张量成像(DTI)对急性期脑梗死进行观察,探讨受累的皮质脊髓束与临床运动功能损害的相互系,评价DTI在判断脑梗死中的价值.资料与方法 对25例超急性、急性期脑梗死患者行DTI检查,对所得的原始数据利用纤维束重组软件行三维皮质脊髓束重组,观察梗死灶与皮质脊髓束的系;并对其行2次临床神经功能症状评分,作为临床评价标准.结果 皮质脊髓束若从梗死灶边缘通过,其可表现无受压、移位、中断,患者的运动症状可表现为无或轻微影响;若皮质脊髓束部分从梗死灶中通过,其可表现部分受压、中断,患者运动功能出现症状,治疗后症状部分恢复;若皮质脊髓束全部从梗死灶中通过,其可表现大部分中断、破坏,临床运动功能表现为大多数运动功能无恢复或轻微改善.结论 通过DTI可对脑梗死治疗效果及预后评估提供重要的功能解剖学依据.     

老年人认知功能与白质异常相关性的MR扩散张量成像研究

目的:本研究利用MR扩散张量成像部分各向异性(FA)值,研究老年人的不同水平认知功能和脑白质异常的相关性,并探讨脑内微静脉改变的意义.方法:正常认知功能(CN)组13例,轻度认知功能障碍(MCI)组12例,痴呆组10例.采用简易智能状态量表(MMSE)、临床痴呆量表(CDR)、总体衰退量表(GDS)和日常生活活动能力量...     

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.     

Accuracy of Diffusion Tensor Imaging for Diagnosing Cervical Spondylotic Myelopathy in Patients Showing Spinal Cord Compression

ObjectiveTo assess the performance of diffusion tensor imaging (DTI) for the diagnosis of cervical spondylotic myelopathy (CSM) in patients with deformed spinal cord but otherwise unremarkable conventional magnetic resonance imaging (MRI) findings.ResultsThe MD, LD, and RD cut-off values were 1.079 × 10^-3, 1.719 × 10^-3, and 0.749 × 10^-3 mm²/sec, respectively, and that of FA was 0.475. Sensitivity, specificity, positive predictive value and negative predictive value were: 100 (4/4), 44.8 (13/29), 20 (4/20), and 100 (13/13) for MD; 100 (4/4), 27.6 (8/29), 16 (4/25), and 100 (8/8) for FA; 100 (4/4), 58.6 (17/29), 25 (4/16), and 100 (17/17) for MD∩FA; 100 (4/4), 68.9 (20/29), 30.8 (4/13), and 100 (20/20) for LD∩FA; and 75 (3/4), 68.9 (20/29), 25 (3/12), and 95.2 (20/21) for RD∩FA in percentage value. Diagnostic performance comparisons revealed significant differences only in specificity between FA and MD∩FA (p = 0.003), FA and LD∩FA (p < 0.001), FA and RD∩FA (p < 0.001), MD and LD∩FA (p = 0.024) and MD and RD∩FA (p = 0.024).ConclusionFractional anisotropy combined with MD, RD, or LD is expected to be more useful than FA and MD for diagnosing CSM in patients who show deformed spinal cords without signal changes on MRI.     

婴幼儿脑白质发育的弥散张量磁共振成像

目的：应用弥散张量成像分析不同年龄段婴幼儿的不同部位脑白质的各向异性。材料和方法：将26例正常婴幼儿（年龄4d至24个月）分为4组：第一组7例，小于6个月；第二组8例，6—12个月；第三组6例，12—18个月；第四组5例，18—24个月。均进行常规头颅MR和弥散张量成像，并测量不同部位脑白质的FA值和ADC值。结果：随着年龄的增加，ADC值逐渐减低，FA值逐渐升高。不同组别大脑白质各部位的ADC值和FA值不同（P〈0．05）。结论：弥散张量成像可以反映活体脑白质的细微结构，可用于评价脑白质发育情况。     

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。     

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。     

苯丙酮尿症脑部病变扩散加权成像

目的 使用磁共振扩散加权成像(DWI)技术研究苯丙酮尿症(phenylketonuria,PKU)患者脑白质内病灶的扩散特点,并观察表观扩散系数(apparent diffusion coefficient,ADC)的变化.资料与方法 对8例临床确诊的PKU患儿及性别、年龄相匹配的8名健康儿童(对照组)行T1WI、T2WI及DWI,测量侧脑室后角T2WI异常信号区及放射冠正常白质的ADC值和对照组相应部位的ADC值.结果 在T2WI上,所有未经治疗的PKU患儿均表现为非占位性、斑片状、条带状高信号,在X、Y、Z 3个方向同时施加扩散梯度的跟踪ADC图(trace APC map)上显示更清晰.患儿大脑白质病灶X、Y、Z 3个方向的ADC值明显低于对照组相应部位脑白质的ADC值,两者差异存在统计学意义(P＜0.05).平均ADC值比对照组相应部位减少23%,侧脑室后角扩散各向异性消失(F=0.195,P=0.825).结论 未经治疗的PKU白质异常在DWIav上显示更清晰,DWI可提供PKU患儿脑白质病灶的病理信息.     

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.     

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。