首页 > 文献资料
-
地黄合剂对多发性硬化患者外周血及脑脊液中T淋巴细胞亚群的影响
多发性硬化(multiple sclerosis, MS)是中枢神经系统原发性脱髓鞘性疾病,病理特点为脑与脊髓的白质中散在的多发性脱髓鞘和继发性胶质增生所形成的硬化斑块.MS的发病机制目前尚未完全清楚,因此,在治疗上仍无特效疗法.1998年1月~2001年6月我们采用地黄合剂治疗MS,取得较好疗效.本研究将着重探讨地黄合剂对MS患者外周血及脑脊液中T淋巴细胞亚群的影响.
-
缓解-复发型多发性硬化患者血脑屏障损害及sICAM-1、TNF-α水平的临床分析
在多发性硬化(multiple sclerosis,MS)及实验性自身免疫性脑脊髓炎(experimental allergic encephalomyelitis,EAE)中,血脑屏障(blood-brain barrier,BBB)受到破坏,淋巴细胞介导BBB损害继而浸润中枢神经系统是MS发病特征之一,而炎症细胞黏附于内皮细胞是其由循环进入脑的第一步.研究表明细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)在脑微血管内皮细胞(BMEC)的表达增加与淋巴细胞黏附和穿越BBB有关,ICAM-1的水平的升高被认为是反映BBB遭到破坏[1]和病情进一步恶化的重要指标.
-
关于多发性硬化脑脊液生物标志物研究中对照组的定义以及实施指南
在多发性硬化(MS)生物标志物的研究中,急需对作为对照组的疾病进行科学合理的定义,包括疾病性质是否与MS的炎症性机制相似、疾病流行病学(如年龄和性别分布等)是否与MS具有可比性等.以往许多研究均未明确哪些疾病作为疾病对照人选,也未明确入选的多种疾病的例数分布.健康对照标本难以取得,同时为了被研究的生物标志物能够更好地用于鉴别诊断以及发现病理方面的特异性,也需要设置疾病对照.鉴于此,BioMS--eu研究网络的12个成员实验室的专家通过指南的方式提出MS脑脊液生物标志物研究中标本的基本信息要求、几种对照组的定义(并列出相应的疾病)以及使用对照组的建议.
-
2012泛北京多发性硬化治疗和研究协作组专家论坛会议纪要
泛北京多发性硬化治疗和研究协作组(Pan Beijing Group of Treatment and Research in Multiple Sclerosis,PBJGTRIMS)论坛,于2012-11-09在福建厦门召开,来自全国各地33位专家与会,会议围绕MS的诊断、鉴别诊断、脑脊液检查、影像学检查和治疗等方面进行了广泛交流和讨论.1 MS诊断 由北京天坛医院神经内科张星虎教授中心发言.诊断MS需同时具备病灶时间多发和中枢神经系统(CNS)空间多发性,并排除其他疾病.
-
国际儿童多发性硬化研究组对儿童多发性硬化和免疫介导的中枢神经系统脱髓鞘疾病的诊断标准:对2007年标准的修订
2007年,国际儿童多发性硬化研究组(International Pediatric Multiple Sclerosis Study Group,IPMSSG)提出了儿童中枢神经系统(CNS)脱髓鞘疾病的诊断标准,包括多发性硬化(MS)、急性播散性脑脊髓炎(ADEM)、视神经脊髓炎(NMO)和临床孤立综合征(CIS),统一了儿童CNS脱髓鞘疾病的术语,为此类疾病的临床和流行病学研究奠定了基础.其后儿童CNS脱髓鞘疾病的研究取得了长足的进展,包括:对儿童ADEM的理解更加充分;更好地明确了能够在儿童CIS后预测MS发病的临床和MRI特征;认识到儿童MS的复发较成人更常见,但进展性起病者较成人罕见;认识到12岁以下发病的儿童的首次发作在临床和影像学方面与更大年龄发病者存在显著不同;更加明确了儿童MS的MRI特点;在儿童更好地界定了NMO和NMO病谱;在对儿童MS患者诊断后就需要疾病修正治疗方面已经达成更加广泛的共识等.
-
Myelin regeneration is indispensably important for patients suffering from several central nervous system (CNS) disorders such as multiple sclerosis (MS) and spinal cord injury (SCI), because it is not only essential for restoring neurophysiology, but also protects denuded axons for secondary degeneration. Understanding the cellular and molecular mechanisms underlying re-myelination is critical for the development of remyelination-speciifc therapeutic approaches. As remyelination shares certain common mechanisms with developmental myelination, knowledge from study of developmental myelination contributes greatly to emerging myelin regeneration therapies, best evidenced as the recently developed human anti-Nogo receptor interacting pro-tein-1 (LINGO-1) monoclonal antibodies to treat MS patients in clinical trials.
-
A preliminary clinical study by our group demonstrated Bushen Yisui Capsule (formerly cal ed Er-huang Formula) in combination with conventional therapy is an effective prescription for the treat-ment of multiple sclerosis. However, its effect on axonal injury during early multiple sclerosis re-mains unclear. In this study, a MOG 35-55-immunized C57BL/6 mouse model of experimental au-toimmune encephalomyelitis was intragastrical y administered Bushen Yisui Capsule. The results showed that Bushen Yisui Capsule effectively improved clinical symptoms and neurological function of experimental autoimmune encephalomyelitis. In addition, amyloid precursor protein expression was down-regulated and microtubule-associated protein 2 was up-regulated. Experimental findings indicate that the disease-preventive mechanism of Bushen Yisui Capsule in experimental autoim-mune encephalomyelitis was mediated by amelioration of axonal damage and promotion of rege-neration. But the effects of the high-dose Bushen Yisui Capsule group was not better than that of the medium-dose and low-dose Bushen Yisui Capsule group in preventing neurological dysfunction.
-
Experimental al ergic encephalomyelitis is a mouse model of human multiple sclerosis with similar pathology and pathogenesis. Th1 cells play an important role in the pathogenesis of experimental al ergic encephalomyelitis. This study determined the potential effect of programmed celldeath 1 ligand 1 in the pathogenesis of experimental al ergic encephalomyelitis induced by injecting myelin oligodendrocyte glycoprotein, complete Freund’s adjuvant and Bordetel a pertussis toxin into C57BL/6J mice. Experimental al ergic encephalomyelitis mice developed disease and showed in-flammatory changes in the central nervous system by hematoxylin-eosin staining of spinal cord pathological sections, demyelination by Luxol fast-blue staining and clinical manifestations. The expression of programmed celldeath 1 ligand 1 in mice was detected by immunohistochemistry, flow cytometry and western blot analysis. The expression of programmed celldeath 1 ligand 1 in the spinal cord and splenocytes of mice was significantly increased compared with normal mice. Our findings suggest the involvement of programmed celldeath 1 ligand 1 in the pathogenesis of expe-rimental al ergic encephalomyelitis and suggest this should be studied in multiple sclerosis.
-
Inflammatory demyelinating pseudotumor usual y occurs in the brain and rarely occurs in the spinal cord. On imaging, inflammatory demyelinating pseudotumor appears very similar to intramedul ary tumors such as gliomas. It is often misdiagnosed as intramedul ary tumor and surgical y resected. In view of this, the clinical and magnetic resonance imaging manifestations and the pathological fea-tures of 36 cases of inflammatory demyelinating pseudotumor in the spinal cord were retrospec-tively analyzed and summarized. Most of these cases suffered from acute or subacute onset and exhibited a sensorimotor disorder. Among them, six cases were misdiagnosed as having intrame-dul ary gliomas, and inflammatory demyelinating pseudotumor was only identified and pathologi-cal y confirmed after surgical resection. Lesions in the cervical and thoracic spinal cord were com-mon. Magnetic resonance imaging revealed edema and space-occupying lesions to varying de-grees at the cervical-thoracic junction, with a predominant feature of non-closed rosette-like rein-forcement (open-loop sign). Pathological examination showed perivascular cuffing of predominantly dense lymphocytes, and demyelination was observed in six of the misdiagnosed cases. These re-sults suggest that tumor-like inflammatory demyelinating disease in the spinal cord is a kind of special demyelinating disease that can be categorized as inflammatory pseudotumor. These solitary lesions are easily confused with intramedul ary neoplasms. Patchy or non-closed reinforcement (open-ring sign) on magnetic resonance imaging is the predominant property of inflammatory de-myelinating pseudotumor, and inflammatory cel infiltration and demyelination are additional patho-logical properties.
-
孤立病灶的脱髓鞘与多发性硬化
复发-缓解型多发性硬化(relapsing-remitting multiple sclerosis, RRMS)活动期可采用激素治疗,缓解期和继发进展期也有干扰素-β(interferon-β)、glatirame和米妥蒽醌等免疫抑制疗法,但尚无充足证据表明它们可以阻止疾病的进展和功能缺损的发生.当患者已经有两次临床发作符合MS诊断标准时,就已经存在了部分不可逆性损害.
-
简评多发性硬化诊断的McDonald标准(2010)和缓解期治疗进展
临床上广泛应用的多发性硬化(multiple sclerosis,MS)McDonald诊断标准制定于2001年,分别于2005年和2010年进行了修改.2010年5月国际MS诊断组在爱尔兰都柏林举行会议,讨论了McDonald诊断标准的应用问题,研讨了McDonald诊断标准在欧洲、亚洲、拉丁美洲MS患者及儿童患者中的应用,并提出了新的修改意见,制定了新的诊断标准(表1)[1].
-
多发性硬化与特发性炎性脱髓鞘疾病诊断的若干问题
多发性硬化(multiple sclerosis,MS)是中枢神经系统(CNS)特发性炎性脱髓鞘疾病(idiopathic inflammatory demyelinating diseases,IIDD)家族的代表和重要的成员,此家族还包括MS变异型(如Marburg型急性MS、Bal6病和Schilder病)、视神经脊髓炎(NMO)、急性播散性脑脊髓炎(ADEM)、临床孤立综合征(CIS)和瘤样炎性脱髓鞘病(TIDD)等[1].
-
醋酸格拉默能够有效延缓临床孤立综合征发展成临床确诊的多发性硬化
背景和目的:醋酸格拉默(glatiramer acetate,GA)已被批准治疗复发缓解型多发性硬化(relapsing remitting multiple sclerosis,RRMS),可以减少其复发率以及通过MRI观察到的疾病活动性和病灶负载.
-
-
中医药治疗多发性硬化的疗效与可能机理
多发性硬化(MS)是中枢神经系统自身免疫反应引起的炎性脱髓鞘病.主要临床特征是反复发作的神经功能障碍,多为复发缓解形式(R-R型),少数为缓慢进展或由R-R型转为进展型.MS的发作频度和病损的严重程度常常难以预先估计.经典的类固醇药物治疗急性发作有效,但不能解决复发和累积性神经功能障碍致残,而且对部分病例和少数进展型疗效不佳甚至无效,因而MS的治疗尚属现代神经病学的一大难题[1].
-
HLA 基因与多发性硬化遗传易感性关系的研究进展
多发性硬化( multiple sclerosis ,MS)是一种常见的神经系统疾病,临床特征以炎性脱髓鞘或伴有轴突损伤为特征。现代认为, MS是环境和遗传共同作用导致变态反应性免疫障碍的多基因遗传性疾病[1]。人类白细胞抗原( human leukocyte antigen ,HLA)基因是目前认为与MS 关联性为肯定的遗传因素,占遗传风险因素的10%~40%[2]。
2005年国际 MS 遗传学联盟( International Multiple Sclerosis Genetics Consortium , IMSGC)通过对730多个成员受累家族中进行的4500个单核苷酸多态性连锁扫描结果,再次肯定了HLA与MS易感性的连锁,而其他非HLA位点则未达到在染色体组范畴上的统计学意义[3]。 -
1例多发性硬化间质干细胞移植治疗的康复护理
多发性硬化(multiple sclerosis,MS)是一种中枢神经系统自身免疫性疾病,主要病理改变为大脑白质的多部位炎症、髓鞘脱失和胶质瘢痕[1].其病因尚不清楚,在具有遗传易感的个体中,病毒感染、内分泌以及环境因素激发的自身免疫机制可能导致发病.
-
视神经脊髓炎和抗水通道蛋白抗体
视神经脊髓炎(neuromyelitis optica,NMO)是一种免疫介导、临床上具有复发或单向病程、选择性损伤视神经和脊髓的中枢神经系统脱髓鞘病.东方人中视神经和脊髓是中枢神经系统脱髓鞘疾病的好发部位.在日本以复发性视神经炎和脊髓炎为特征,脑部几乎不受累或很少受累的一类独特的脱髓鞘疾病,称为视神经脊髓炎型多发性硬化(optieospinal multiple sclerosis,OSMS)或者亚洲型多发性硬化(multiple sclerosis,MS),其临床特征与复发型NMO类似[1,2].
-
大剂量甲基强的松龙促进多发性硬化患者锥体系功能恢复36例
BACKGROUND:In China,steroid such as dexamethasone was often used for curing multiple sclerosis(MS),which had definitive effect but was slow in effect and needed a long time for taking medicine,more importantly,had severe side- effect.In recent years,high dose methylprednisolone has achieved some effect on immuno- neurologic diseases.
-
儿童多发性硬化发病机制和诊断治疗研究进展
多发性硬化(multiple sclerosis,MS)为慢性、复发性、多病灶性中枢神经系统白质脱髓鞘病.MS在美国的发病率为100/10万[1],英国为127/10万.儿童病例少见,10岁以下MS儿童占MS的0.2%~2.0%,近年发现MS发病有增多趋势.女性多见,尤其是儿童病例.