缺血性脑卒中合并多发性硬化患者血清Omentin-1、MMP-9水平检测的意义

目的探讨缺血性脑卒中合并多发性硬化患者血清网膜素-1(Omentin-1)、基质金属蛋白酶-9(MMP-9)水平检测的意义。方法选取2013年9月至2015年9月期间该院确诊治疗的缺血性脑卒中患者169例作为患者组,又依据是否合并多发性硬化分为合并组(n=57例)和单病组(n=112例)。另外,选取同期于该院体检中心进行体检的健康者30例作为健康组。所有纳入研究者均采用酶联免疫吸附测定(ELISA)检测血清Omentin-1、MMP-9水平,统计并分析所有纳入研究者血清Omentin-1、MMP-9水平和神经功能情况。结果患者组血清MMP-9水平和扩展功能障碍状态量表(EDSS)得分明显高于健康组(P0.05),前者血清Omentin-1水平明显低于后者(P0.05)。合并组患者血清MMP-9水平和扩展功能障碍状态量表(EDSS)得分明显高于单病组,前者血清Omentin-1水平明显低于后者,差异有统计学意义(P0.05)。Pearson相关性分析显示,血清Omentin-1水平与EDSS得分呈负相关(r=-0.724,P0.05),血清MMP-9水平与EDSS得分呈正相关(r=0.763,P0.05);Logistics回归性分析显示,血清低Omentin-1水平和高MMP-9水平及高EDSS得分是缺血性脑卒中合并多发性硬化的独立危险因素(P0.05);受试者工作特征曲线(ROC)曲线分析结果显示,血清Omentin-1以180ng/mL为临界值时,血清MMP-9以260ng/mL为临界值时,二者联合用于预测缺血性脑卒中患者合并多发性硬化的敏感度、特异度、准确度分别为94.74%、96.43%、95.86%。结论血清Omentin-1、MMP-9水平与缺血性脑卒中合并多发性硬化的发生有关,也是后者发生的独立危险因素,而且可以有效评估患者的神经功能残疾情况,联合检测上述指标的水平可有效协助医师评估患者的病情变化及预测缺血性脑卒中患者合并多发性硬化的发生,值得临床作进一步推广。     

多发性硬化76例MRI诊断分析

目的探讨多发性硬化(MS)的MRI表现及其诊断价值。方法回顾性分析76例诊断多发性硬化(MS)患者的临床与MRI资料。结果病灶主要分布于侧脑室周围占90.1%,大小以<1 cm最多占81.2%。病灶信号以稍长T1,长T2为主,增强呈不均匀斑片状或环状强化。MRS上陈旧性病灶NAA峰下降,急性期病灶NAA峰下降,胆碱峰、脂质峰及乳酸峰升高。结论 MRI对多发性硬化的诊断具有重要价值。     

STAyCIS研究:大剂量阿托伐他汀可减少临床孤立综合征患者头MRI新发T2病灶数量

他汀类药物为临床常用的降脂药物,体外及体内的诸多研究表明,他汀类药物具有免疫调节作用。多发性硬化的实验模型研究中,口服他汀类药物可以通过异戊二烯化ras和rho三磷酸酶刺激T细胞分化,从而阻止炎性反应的复发或者转复肢体的无力。2004年《柳叶刀》杂志Vollmer等学者曾经报道辛伐他汀可以减少多发性硬化患者头MRI的新发T2病灶数量。之后有关多发性硬化的治疗研究,多为他汀类药物结合β-干扰素-1a进行。但是在联合β-干扰素-1a治疗的同时,他汀类药物没有和     

脑内多发性硬化46例MRI表现分析

目的:分析脑内多发性硬化MRI表现特点,提高MRI对该病的诊断水平.方法:分析46例经临床证实的脑内多发性硬化MRI表现,对病灶的形态、分布、数目、大小、信号及强化进行分析.结果:脑内多发性硬化MRI特征性表现为双侧半卵圆中心、双侧脑室旁白质内、胼胝体及中脑不规则形多发病灶,其中侧脑室旁病灶长轴垂直于侧脑室,病变在急性或活动期有强化.结论:MRI是目前诊断脑内多发性硬化的最佳影像检查方法.     

脑型多发性硬化的磁共振影像学分析

目的:探讨脑型多发性硬化(MS)的临床特点,分析核磁共振检查(MRI)对脑型多发性硬化的诊断价值。方法:搜集脑型多发性硬化患者的MRI结果进行回顾性分析。结果:23例患者入组,脑MRI检查均有阳性发现,以脑室周围及胼胝体最常受累,皮质受累4例(17.4%)。MRI增强见强化病灶者13例(56.5%)。结论:常规MRI对多发性硬化的诊断具有一定的价值,必要时定期复查。     

复发好转型多发性硬化磁化传递成像研究

目的利用磁化传递率(MTR)直方图分析,研究复发好转型多发性硬化(RRMS)脑异常改变及MTR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例正常志愿者行T2WI和磁化传递成像检查,计算出每个体素的MTR值后,绘制出全脑MTR直方图并对其进行分析.结果 RRMS患者的全脑MTR直方图明显左移,峰高降低.RRMS患者的全脑平均MTR [(29.45±1.83)%]明显低于正常志愿者[(30.37±1.37)%](P=0.025),MTR直方图峰位置[(32.51±2.02)%]也明显低于正常志愿者[(33.51±1.39)%](P=0.022).在RRMS患者,全脑MTR直方图峰高与EDSS评分中度相关 (r=-0.411, P=0.027).结论脑MTR直方图分析可显示RRMS患者脑异常改变,脑MTR直方图峰高可用于监测该病的临床进展.     

多发性硬化的磁共振波谱研究

目的研究多发性硬化(MS)患者脑内病灶、表现正常脑白质(NAWM)及正常志愿者脑白质的代谢差异,并探讨代谢物浓度比值与临床残疾程度的相关性。方法对32例MS患者和25例正常志愿者进行MRI和质子磁共振波谱(1H MRS)检查,测量各感兴趣区的代谢产物氮-乙酰天冬氨酸(NAA)、肌酸(Cr)及胆碱(Cho)的浓度比率,并分析NAA/Cr及NAA/Cho与扩展残疾状态量表(EDSS)的相关性。结果MS患者的病灶内NAA/Cr及NAA/Cho显著低于NAWM(P<0.001),NAWM的NAA/Cr及NAA/Cho亦显著低于正常对照组(P<0.001)。MS患者病灶和NAWM的NAA/Cr及NAA/Cho与EDSS均无显著相关性。结论1H MRS能检测出MS患者脑部病灶及NAWM的代谢异常,为常规MRI提供补充信息。     

多发性硬化患者社会参与能力及影响因素分析

目的探讨多发性硬化患者社会参与能力及其影响因素,为促进多发性硬化患者的临床干预及管理提供参考。方法采用一般资料问卷、中文版参与和自主性测评问卷(IPA)、扩展残疾状况评分(EDSS)、焦虑自评量表(SAS)及抑郁自评量表(SDS)对80例多发性硬化患者进行调查,并采用多重线性回归分析其社会参与能力的影响因素。结果多发性硬化患者社会参与能力总分为(51.18±21.50)分,社会参与各维度中,室外自主性参与最差。EDSS、SAS评分、SDS评分、病程与社会参与总分及各维度之间呈正相关(P均<0.05),家庭人均月收入与社会参与总分及各维度得分呈负相关(P均<0.05),复发次数与社会参与总分、家庭角色、室外自主参与和社会生活自主参与得分呈正相关(P均<0.05)。EDSS、SAS评分、家庭人均月收入及病程是MS患者社会参与能力的影响因素。结论多发性硬化患者社会参与能力总体处于较差水平。临床工作者应以社会参与各影响因素为切入点对患者实施个体化的、有针对性的康复干预及心理干预,适度提升其社会参与能力,改善其生存质量。     

中国经典型多发性硬化患者β干扰素-1b治疗前后血清尿酸水平

  目的  探讨中国经典型多发性硬化(classical multiple sclerosis, CMS)患者β干扰素-1b治疗前后血清尿酸(uric acid, UA)水平的变化及其与复发率、扩展残疾状态评分(Expanded Disability Status Scale, EDSS)和颅内增强病灶(contrast-enhancing lesions, CELs)数目间的关系。  方法  12例CMS患者(10例女性, 2例男性, 年龄:24~54岁)被纳入至一项为期6个月的疗效观察研究。在疾病缓解期, 给予β干扰素-1b(250 μg, 皮下注射, 隔日1次)治疗。治疗前后评估患者EDSS评分、年复发次数、颅内CELs数目和血清UA水平。  结果  治疗后, 患者年复发次数(0.0比0.9, P=0.011)和颅内CELs数目(0.0比1.5, P=0.007)较治疗前明显减低; EDSS评分有降低趋势(2.0比2.8), 但差异无统计学意义(P=0.064);血清UA水平从222.2 μmol/L升高至234.9 μmol/L, 但差异亦无统计学意义(P=0.213)。进一步研究发现, 血清UA水平升高与颅内CELs数目减低显著相关(r=-0.716, P=0.009)。  结论  血清UA水平有可能成为评估CMS患者对β干扰素-1b治疗反应的一个监测指标。     

肌电生物反馈联合康复训练对多发性硬化患者下肢肌肉痉挛和步行功能的影响

目的 前瞻性分析肌电生物反馈联合康复训练治疗对多发性硬化患者的下肢痉挛状态、步行能力和残疾水平的影响。 方法 选取下肢痉挛的多发性硬化患者73例，采用随机数字表法将其分为对照组（36例）和治疗组（37例）。2组患者均给予常规康复训练，治疗组在此基础上应用肌电生物反馈进行辅助训练，共4周。分别于治疗前和治疗后，采用改良的Ashworth量表(MAS)、Holden步行功能分级（FAC）和功能残疾扩展量表(EDSS)分别评价2组患者的痉挛程度、步行能力及残疾水平。 结果 2组患者治疗后的MAS分级、FAC分级及EDSS评分［对照组(3.36±1.06)、(4.03±1.64)和(5.03±1.39)分；治疗组(2.74±1.05)、(4.12±1.57)和(3.98±1.53)分］均明显优于组内治疗前评分［对照组(4.11±1.02)、(3.11±1.38)和(6.21±1.57)分；治疗组(4.21±1.13)、(3.07±1.27)和(6.07±1.15)分］，且差异均有统计学意义(P<0.05)。治疗后，治疗组MAS分级和EDSS评分明显优于对照组，且组间差异有统计学意义(P<0.05)；而治疗后FAC分级评分组间比较，差异无统计学意义(P>0.05)。 结论 肌电生物反馈联合康复训练治疗可显著改善多发性硬化患者的下肢肌痉挛程度和残疾水平。     

The relationship between whole brain volume and disability in multiple sclerosis: a comparison of normalized gray vs. white matter with misclassification correction

We used SPM99 to obtain normalized whole brain volumes of gray matter, white matter, and total parenchyma in patients with multiple sclerosis (MS) (n = 41) and age-/sex-matched normal controls (n = 18). As SPM99's automated gray/white matter volumes were significantly influenced by tissue compartment misclassification due to the effect of MS-related brain lesions, we corrected these automated volumes for misclassification before performing our primary analyses. For MS patients (disease duration = 9.5 +/- 6.3 years; EDSS score = 3.2 +/- 1.8; 25FTW = 6.6 +/- 3.1 s), we also measured lesion load (total T1 hypointense [T1LV] and FLAIR hyperintense lesion volume [FLLV]), central brain atrophy (third ventricular width [TVW] and bicaudate ratio [BCR]), and clinical status (Expanded Disability Status Scale [EDSS] and 25-ft timed walk [25FTW]). Patients with MS had lower gray matter (707 +/- 33 cm(3) [-3.9%], P = 0.003) and total parenchymal volume (1088 +/- 48 cm(3) [-3.8%], P = 0.003), but only a trend for lower white matter volume (381 +/- 25 cm(3) [-3.7%], P = 0.052) relative to normal controls (gray matter: 736 +/- 33 cm(3); total parenchyma: 1132 +/- 49 cm(3); white matter: 396 +/- 26 cm(3)). Gray matter atrophy was related to clinical status (EDSS, 25FTW, and disease duration), lesion load (T1LV and FLLV), and central brain atrophy (TVW and BCR), whereas white matter atrophy was related to only central brain atrophy. These findings suggest that gray matter loss is related to other aspects of brain pathology and has more clinical relevance than white matter atrophy in MS.     

Independent contributions of cortical gray matter atrophy and ventricle enlargement for predicting neuropsychological impairment in multiple sclerosis

The primary goal of this study was to investigate associations between regional gray matter (GM) atrophy and neuropsychological function in multiple sclerosis (MS), while accounting for the influence of central brain atrophy (i.e. third ventricle enlargement). Using a cross-sectional design, we studied 59 MS patients with brain MRI and neuropsychological testing. Regional gray matter fractions (rGMFs) were calculated from MRI images for 11 homologous brain areas using the semiautomatic brain region extraction (SABRE) technique. Neuropsychological testing followed consensus panel guidelines and included tests emphasizing episodic memory, working memory and processing speed. The analytic approach was stepwise linear regression, with forward selection and p<0.05 threshold for significance. Consistent with previous research, there were significant correlations between third ventricle width and neuropsychological tests. Stepwise linear regression analyses controlling for third ventricle width retained rGMFs obtained from specific regions within the prefrontal cortex. Left frontal atrophy was associated with tests emphasizing auditory/verbal memory. Right frontal atrophy was associated with impairment in visual episodic and working memory. For the first time, we show an independent relationship between cortical atrophy and cognitive impairment after accounting for the effects of central atrophy.     

Immunoadsorption patients with multiple sclerosis: an open-label pilot study

BACKGROUND: Immunoadsorption (IA) is occasionally applied in patients with acute relapses of multiple sclerosis (MS). This pilot study was undertaken to determine whether IA might help in secondary progressive and relapsing-remitting multiple sclerosis. DESIGN: IA was performed at 1-week intervals in 12 patients with secondary progressive or relapsing-remitting MS. These patients had an extended disability status scale (EDSS) score of 4.5-7 and an EDSS increase of 0.5 within 6 months before inclusion in the study despite conventional drug therapy. The change in the EDSS and that in the MS functional composite (MSFC) score, which consisted of quantitative tests of arm function, ambulation, visual acuity and cognition, served as the primary outcome variables, which were measured at baseline and at 3, 6 and 12 months. Changes in quality of life and cerebral lesions by magnetic resonance imaging (MRI) were also assessed at baseline and after the last immunoadsorption (month 3). RESULTS: A significant reduction of the median EDSS change was observed after the treatment period, which reversed 3 months after the immunoadsorptions had been stopped. Ten of 12 patients remained stable during the first year of follow-up with no significant changes of the MSFC scores. No significant changes in magnetic resonance imaging T2-hyperintense brain lesions or in the number of gadolinium-positive lesions and in the patients' quality of life were observed. Western blot analyses demonstrated a reduction of serum myelin-specific antibodies, which were collected in the adsorber eluates. CONCLUSIONS: Removal of immunoglobulins, including myelin-specific antibodies by immunoadsorption, seems to delay disease progression as defined by EDSS, MSFC and MRI, while the patients' quality of life did not deteriorate.     

Regional brain atrophy development is related to specific aspects of clinical dysfunction in multiple sclerosis

Brain atrophy in multiple sclerosis (MS) is thought to reflect irreversible tissue damage leading to persistent clinical deficit. Little is known about the rate of atrophy in specific brain regions in relation to specific clinical deficits. We determined the displacement of the brain surface between two T1-weighted MRI images obtained at baseline and after a median follow-up time of 2.2 years for 79 recently diagnosed, mildly disabled MS patients. Voxel- and cluster-wise permutation-based statistics were used to identify brain regions in which atrophy development was significantly related to Expanded Disability Status Scale (EDSS), Timed Walk Test (TWT), Paced Auditory Serial Addition Test (PASAT) and 9-Hole Peg Test (HPT). Clusters were considered significant at a corrected cluster-wise p-value of 0.05. Worse EDSS change-score and worse follow-up EDSS were related to atrophy development of periventricular and brainstem regions and right-sided parietal, occipital and temporal regions. Worse PASAT at follow-up was significantly related to atrophy of the ventricles. A worse TWT change-score and worse follow-up TWT were exclusively related to atrophy around the ventricles and of the brainstem. Worse HPT change-score and worse follow-up HPT of either arm were significantly related to the atrophy of widely distributed peripheral regions, as well as atrophy of periventricular and brainstem regions. Our findings suggest that decline in ambulatory function is related to atrophy of central brain regions exclusively, whereas decline in neurologically more complex tasks for coordinated hand function is related to atrophy of both central and peripheral brain regions.     

Deficient MWF mapping in multiple sclerosis using 3D whole-brain multi-component relaxation MRI

Recent multiple sclerosis (MS) MRI research has highlighted the need to move beyond the lesion-centric view and to develop and validate new MR imaging strategies that quantify the invisible burden of disease in the brain and establish much more sensitive and specific surrogate markers of clinical disability. One of the most promising of such measures is myelin-selective MRI that allows the acquisition of myelin water fraction (MWF) maps, a parameter that is correlated to brain white matter (WM) myelination. The aim of our study was to apply the newest myelin-selective MRI method, multi-component Driven Equilibrium Single Pulse Observation of T1 and T2 (mcDESPOT) in a controlled clinical MS pilot trial. This study was designed to assess the capabilities of this new method to explain differences in disease course and degree of disability in subjects spanning a broad spectrum of MS disease severity. The whole-brain isotropically-resolved 3D acquisition capability of mcDESPOT allowed for the first time the registration of 3D MWF maps to standard space, and consequently a formalized voxel-based analysis of the data. This approach combined with image segmentation further allowed the derivation of new measures of MWF deficiency: total deficient MWF volume (DV) in WM, in WM lesions, in diffusely abnormal white matter and in normal appearing white matter (NAWM). Deficient MWF volume fraction (DVF) was derived from each of these by dividing by the corresponding region volume. Our results confirm that lesion burden does not correlate well with clinical disease activity measured with the extended disability status scale (EDSS) in MS patients. In contrast, our measurements of DVF in NAWM correlated significantly with the EDSS score (R² = 0.37; p < 0.001). The same quantity discriminated clinically isolated syndrome patients from a normal control population (p < 0.001) and discriminated relapsing-remitting from secondary-progressive patients (p < 0.05); hence this new technique may sense early disease-related myelin loss and transitions to progressive disease. Multivariate analysis revealed that global atrophy, mean whole-brain myelin water fraction and white matter atrophy were the three most important image-derived parameters for predicting clinical disability (EDSS). Overall, our results demonstrate that mcDESPOT-defined measurements in NAWM show great promise as imaging markers of global clinical disease activity in MS. Further investigation will determine if this measure can serve as a risk factor for the conversion into definite MS and for the secondary transition into irreversible disease progression.     

多发性硬化脑内磁共振病灶分布及其特征

目的了解多发性硬化( multiple sclerosis, MS)的病灶特点. 方法选择确诊的缓解-复发型 MS患者 203例,每 6个月检查头颅 MRI一次. 结果① 203例 MS患者中, 172( 84.7%)例脑 MRI显示脱髓鞘病灶.其中有胼胝体病灶者 90例( 52%),有脑干病灶者 106例( 62%),有小脑病灶者 46例( 28%),有与脑室联结的病灶者 157例( 91%),有典型的卵圆形病灶者 98例( 57%),病灶长轴与侧脑室切线垂直的病灶占总病灶一半以上的 130例( 76%).② 203例 MS患者中,大脑半球内和脑内无病灶者分别为 41例 (20% )和 31例 (15% ).仅脑干有病灶者 6例( 3%),仅小脑有病灶者 2例( 1%),脑干和小脑都有病灶者 2例( 1%).③ 203例共检查 827次 MRI,有活动病灶者 77例( 41%),共有活动病灶 261个,分布在大脑、小脑和脑干者依次为 223、 10和 28个. 结论①在确诊 MS患者中,多数脑 MRI有脱髓鞘病灶.②脑内有病灶者中,小脑有病灶者,较欧美报道为低.③ T2像发现活动病灶的机率不高,多次复查能提高病灶的检出率.     

In vivo evidence of disseminated subpial T2* signal changes in multiple sclerosis at 7 T: a surface-based analysis

Cortical subpial demyelination is frequent in multiple sclerosis (MS) and is closely associated with disease progression and poor neurological outcome. Although cortical lesions have been difficult to detect using conventional MRI, preliminary data using T2*-weighted imaging at ultra-high field 7T MRI showed improved sensitivity for detecting and categorizing different histological types of cortical MS lesions. In this study we combined high-resolution 7T MRI with a surface-based analysis technique to quantify and map subpial T2*-weighted signal changes in seventeen patients with MS. We applied a robust method to register 7T data with the reconstructed cortical surface of each individual and used a general linear model to assess in vivo an increase in subpial T2*-weighted signal in patients versus age-matched controls, and to investigate the spatial distribution of cortical subpial changes across the cortical ribbon. We also assessed the relationship between subpial T2* signal changes at 7T, Expanded Disability Status Scale (EDSS) score and white matter lesion load (WMLL). Patients with MS showed significant T2*-weighted signal increase in the frontal lobes (parsopercularis, precentral gyrus, middle and superior frontal gyrus, orbitofrontal cortex), anterior cingulate, temporal (superior, middle and inferior temporal gyri), and parietal cortices (superior and inferior parietal cortex, precuneus), but also in occipital regions of the left hemisphere. We found significant correlations between subpial T2*-weighted signal and EDSS score in the precentral gyrus (ρ=0.56, P=0.02) and between T2*-weighted signal and WMLL in the lateral orbitofrontal, superior parietal, cuneus, precentral and superior frontal regions. Our data support the presence of disseminated subpial increases in T2* signal in subjects with MS, which may reflect the diffuse subpial pathology described in neuropathology.     

Grey and white matter atrophy in early clinical stages of primary progressive multiple sclerosis

BACKGROUND: There is little information available on grey and white matter (GM and WM) atrophy in primary progressive multiple sclerosis (PPMS) and on their relationships with clinical and other magnetic resonance imaging (MRI) measures. AIM: To evaluate disease progression in the early phase of PPMS, focusing on axonal loss as assessed by volumetric MRI measures of WM and GM, and to determine their relationships with clinical outcomes and lesion load measures. METHODS: Forty-three patients with PPMS within 5 years of symptom onset and 45 control subjects were studied. Three-dimensional brain scans were acquired and segmented into WM, GM, and cerebrospinal fluid (CSF) using SPM99. Brain parenchymal (BPF), WM (WMF), and GM fractions (GMF) normalized against total intracranial volumes were estimated. T2-weighted (T2) and enhancing lesion loads were also determined. Expanded Disability Status Scale (EDSS) and Multiple Sclerosis Functional Composite (MSFC) scores were recorded in all patients. RESULTS: There were significant differences between patients and controls in BPF, WMF, and GMF values (P < 0.001). BPF (r = -0.469; P = 0.002) and WMF (r = -0.532; P < 0.001) but not GMF (r = -0.195; P = 0.2) correlated with EDSS scores. BPF (r = 0.518; P = 0.001), WMF (r = 0.483; P = 0.001), and GMF (r = 0.337; P = 0.031) correlated with MSFC scores. Correlations with enhancing lesion and T2 loads were only significant for BPF and WMF. CONCLUSIONS: Brain atrophy is seen in the early stages of PPMS and affects both GM and WM. WM atrophy appears more closely related to clinical outcome and WM focal damage than GM atrophy in this patient group.     

T2 relaxometry can lateralize mesial temporal lobe epilepsy in patients with normal MRI

In unselected patients with intractable temporal lobe epilepsy (TLE), approximately 15% do not have detectable hippocampal atrophy on MRI. The purpose of this study was to evaluate whether T2 relaxometry can identify hippocampal pathology and lateralize the epileptic focus in patients with intractable TLE, who do not demonstrate hippocampal atrophy on volumetric MRI (MRIV). We selected 14 patients with unilateral TLE who had unilateral atrophy and 11 patients with unilateral TLE who had no evidence of atrophy on MRIV. Images were acquired on a 1.5 T MR scan using a dual echo sequence with 23 contiguous oblique coronal slices in all patients and in 14 healthy subjects. Fitting a single exponential decay equation to the imaging data generated T2 maps. Averages of six slices containing the head, body, and tail of the hippocampus were used to calculate hippocampal T2 relaxation times (HT2). The epileptic focus was defined by history, video-EEG, and surgical response. All TLE patients with hippocampal atrophy and 9/11 (82%) patients with normal MRI had abnormally high HT2 ipsilateral to the epileptic focus. Bilateral abnormal HT2 were found in 6/14 (43%) of patients with unilateral hippocampal atrophy and 2/11 (18%) of patients with normal MRI. However, this increase was always greater ipsilateral to the epileptic focus. Qualitative hippocampal pathology showed gliosis and neuronal loss in 10/14 operated patients with hippocampal atrophy on MRIV and in 5/7 operated patients with normal MRI. In conclusion, hippocampal T2 mapping provides evidence of hippocampal damage in the majority of patients with intractable TLE who have no evidence of atrophy on MRI and can correctly lateralize the epileptic focus in most patients.     

Quantitative diffusion weighted imaging measures in patients with multiple sclerosis

Diffusion-weighted imaging (DWI) has been proposed as a sensitive measure of disease severity capable of detecting subtle changes in gray matter and white matter brain compartments in patients with multiple sclerosis (MS). However, DWI has been applied to the study of MS clinical subtypes in only a few studies. The objective of this study was to demonstrate the validity of a novel, fully automated method for the calculation of quantitative DWI measures. We also wanted to assess the correlation between whole brain (WB)-DWI variables and clinical and MRI measures of disease severity in a large cohort of MS patients. For this purpose we studied 432 consecutive MS patients (mean age 44.4+/-10.2 years), 16 patients with clinically isolated syndrome (CIS) and 38 normal controls (NC) using 1.5 T brain MRI. Clinical disease subtypes were as follows: 294 relapsing-remitting (RR), 123 secondary-progressive (SP) and 15 primary-progressive (PP). Mean disease duration was 12+/-10 years. Mean Expanded Disability Status Scale (EDSS) was 3.3+/-2.1. Brain parenchymal fraction (BPF), gray matter fraction (GMF) and white matter fraction (WMF) were calculated using a fully automated method. Mean parenchymal diffusivity (MPD) maps were created. DWI indices of peak position (PP), peak height (PH), MPD and entropy (ENT) were obtained. T2- and T1-lesion volumes (LV), EDSS, ambulation index (AI) and nine-hole peg test (9-HPT) were also assessed. MS patients had significantly lower BPF (d=1.26; p<0.001) and GMF (d=0.61; p=0.003), and higher ENT (d=1.2; p<0.0001), MPD (d=1.04; p<0.0001) and PH (d=0.47; p=0.045) than NC subjects. A GLM analysis, adjusted for age and multiple comparisons, revealed significant differences between different clinical subtypes for BPF, GMF, ENT, PH, PP, T2-LV and T1-LV (p<0.0001), WMF (p=0.001) and MPD (p=0.023). In RR and SP MS patients, ENT showed a more robust correlation with other MRI (r=0.54 to 0.67, p<0.0001) and clinical (r=0.31 to 0.36, p<0.0001) variables than MPD (r=0.23 to 0.41, p<0.001 for MRI and r=0.13 to 0.18; p=0.006 to p<0.001 for clinical variables). The GMF and BPF showed a slightly stronger relationship with all clinical variables (r=0.33 to 0.48; p<0.0001), when compared to both lesion and DWI measures. ENT (R2=0.28; p<0.0001) and GMF (R2=0.26; p<0.001) were best related with SP disease course. This study highlights the validity of DWI in discerning differences between NC and MS patients, as well as between different MS subtypes. ENT is a sensitive marker of overall brain damage that is strongly related to clinical impairment in patients with SP MS.