BAEP和TCD在早期诊断后循环缺血中的应用价值

目的研究脑干听觉诱发电位(BAEP)和经颅多普勒超声(TCD)检查在后循环缺血早期诊断中的应用价值。方法 2012-01—2012-12淮南东方医院集团总院神经内科收治62例经磁共振血管成像(MRA)确诊的后循环缺血患者,分别进行BAEP和TCD检查观察是否有相应改变,进而明确该两项检查应用于后循环缺血的诊断价值。结果 62例后循环缺血患者中,BAEP异常58例,异常率95.5%;TCD异常54例,异常率87%。结论 BAEP和TCD的异常对早期诊断后循环缺血有意义。     

89例后循环缺血患者脑血管造影诊断结果分析

目的对确诊为后循环缺血的患者进行数字减影脑血管造影(DSA)检查,分析其病因及DSA对后循环缺血的意义。方法选取2013-01—2014-11间我院收治的后循环缺血患者89例,所有患者均进行DSA检查,分析其在病因判断中的意义。结果 89例后循环缺血患者中67例(75.28%)存在后循环血管异常,其中后循环短暂性脑缺血发作(TIA)27例(40.30%);后循环脑梗死40例(59.70%),2组间血管异常率差异无统计学意义(P0.05)。67例患者共发现病变部位106处,病变类型分别为粥样硬化38例,狭窄47例,闭塞13例,先天异常8例。后循环脑梗死脑血管狭窄率显著高于后循环TIA组(P0.05),但2组间血管狭窄分布无明显差异(P0.05)。结论大部分后循环缺血患者存在后循环血管病变,DSA检查对后循环缺血的诊断具有积极意义。     

彩色多普勒超声仪检查与CT血管成像对后循环缺血的诊断价值

目的 探讨彩色多普勒超声仪(CDFI)检查和多层螺旋CT血管成像(CTA)对后循环缺血的诊断价值.方法 对后循环缺血的40例患者行CDFI和CTA检查,并对结果进行对比.结果 CDFI检查的阳性率为90%(36例),CTA检查阳性率为92.5%(37例),两者比较差异无统计学意义.其中CDFI检测显示椎动脉走形扭曲16例,椎动脉狭窄12例,椎动脉内膜斑块7例,椎动脉缺如1例;CTA显示椎动脉异常29例,基底动脉异常8例.结论 CDFI和CTA检查两种检查方法从不同角度反映了椎动脉血管形态及血流学变化,二者合用,有助于全面客观诊断后循环缺血.     

后循环缺血患者血管形态及支架成形术的疗效

目的探讨后循环缺血患者血管形态及支架成形术的治疗效果。方法选取本院收治的132例后循环缺血患者进行数字减影血管造影检查,并对其中40例后循环血管狭窄严重患者进行支架成形术治疗。结果 132例患者中发现存在颈及颅内血管结构异常者116例,其中单纯前循环病变28例(24.14%),单纯后循环病变52例(44.83%),前后循环均病变36例(31.03%);40例病情较严重患者进行了支架成形术,手术成功率100%,术后患者后循环缺血症状分别在1~10d内明显好转。结论数字减影血管造影对后循环缺血患者的诊断具有非常重要价值,结合支架成形术可有效治疗后循环缺血。     

45例后循环缺血病人头颈部CTA结果分析

目的 通过回顾性分析45例后循环缺血头颈部CTA检测结果,提高临床医师对后循环缺血病因的认识,减少诊断和治疗的混乱.方法 收集临床拟诊为后循环缺血患者,行16排螺旋CT头颈部的检测,观察前循环、后循环系统及颈椎CT的检测结果有无血管的先天变异,血管扭曲受压,血管狭窄、斑块的形成,横突孔有无狭窄及骨赘形成.结果 45例后循环缺血病人头颈部CTA血管病变阳性率88.9%,单纯前循环血管病变11例(24.4%),单纯后循环血管病变3例(6.7%),前后循环均有病变26例(57.8%);单侧横突孔先天狭窄11例,仅2例因为骨赘的形成导致椎动脉受压扭曲变形. 结论 动脉粥样硬化为后循环缺血的最常见病因,前循环缺血也可能是导致病人发生后循环缺血症状的病因,颈椎病不是后循环缺血的主要病因.     

后循环缺血研究进展

近些年,专家共识认为后循环缺血（posterior circulation ischemia,PCI）包括后循环短暂性脑缺血发作（transient ischemic attack,TIA）和后循环梗死。后循环缺血常见的病因为动脉粥样硬化、栓子脱落、锁骨下动脉盗血综合征等;典型的临床表现为眩晕,并常伴有脑干、小脑部位的症状体征;诊断主要依靠详细的病史、查体和神经放射影像学检查;治疗以药物治疗为主,可辅助外科手术治疗和血管内治疗。本文结合近十年来国内外发表的文献从后循环缺血流行病学、常见病因、临床特征、诊断、治疗及预后等方面进行阐述。     

323例后循环缺血患者临床分析

目的探讨后循环缺血的危险因素、临床表现、发病机制及预后。方法通过头颅MRI、MRA、TCD、心电图、颈部多普勒超声、心脏超声等检查,分析后循环缺血的危险因素、血管病变类型、临床特点及预后。结果 323例后循环缺血患者中,274例有不同程度血管狭窄,215例患者有梗死病灶;最常见的临床表现分别是眩晕、共济失调、肢体瘫痪、构音或吞咽障碍;最常见的危险因素依次为高血压、糖尿病等。结论头颅MRI、MRA是检查后循环缺血简便有效的方法,后循环缺血同前循环缺血一样,不容忽视。     

后循环缺血的功能影像学及电生理学研究进展

<正>后循环缺血包括后循环短暂脑缺血发作和后循环脑梗死,约占缺血性脑血管病的20%[1]。功能影像学及电生理学的发展和应用,提高了后循环缺血诊断的正确率。一、后循环缺血的功能影像学研究1.磁共振弥散加权成像(diffusion weighted imaging,DWI)DWI通过快速序列和梯度脉冲来测量分子的净位移,反映     

后循环缺血性卒中的影像学及相关临床表现

本综述回顾了关于后循环不同区域和不同血管分支发生缺血性卒中的临床特征的新近认识,同时复习了近年来关于影像学检查在后循环缺血性卒中的早期诊断能力和对后循环血管状况评估能力的研究观点。     

后循环缺血性眩晕的影像学对照分析

目的探讨CT、磁共振动脉成像(MRA)检查对于后循环缺血性眩晕的诊断价值。方法选取临床表现为后循环缺血性眩晕的患者40例接受CT、MRA及数字减影血管造影(DSA)检查,以DSA检查结果作为金标准,探讨CT、MRA诊断后循环缺血眩晕的诊断学价值。结果40例后循环缺血性眩晕患者,CT检查发现脑梗死病灶患者11例,检出率为27.50%。MRA检查,双侧椎动脉A型44条,B型8条,C型9条,D型9条,正常14条;基底动脉:A型24条,B型4条,C型6条,正常6条;MRA诊断后循环缺血性眩晕的灵敏度为93.27%,特异度为81.25%,漏诊率为6.73%,误诊率为18.75%;CT诊断后循环缺血性眩晕的灵敏度为27.78%,特异度为75.00%,漏诊率为72.22%,误诊率为25.00%。结论 MRA检查对于后循环缺血性眩晕具有较高的诊断价值,且具有无创性的优点。     

神经调控技术治疗抽动秽语综合征研究进展

抽动秽语综合征是一种通常在儿童期起病,以运动及发生抽动为特点的慢性复杂性神经精神疾病,常伴有行为和精神症状,如强迫观念与行为、注意缺陷多动障碍、学习困难、情绪障碍、自伤和猥亵行为等。     

脑血管反应性与缺血性卒中

目的观察缺血性卒中患者脑血管反应性（CVR）变化,确定两者之间的相关性。方法采用经颅多普勒超声（TCD）结合屏气试验检测76例缺血性卒中患者及62例对照病例的屏气指数（BHI）。结果缺血性卒中患者组的BHI明显低于对照组（P〈0.001）,Logistic 回归显示,由BHI所表示的CVR是缺血性卒中的独立影响因素（P=0.000）。结论降低的CVR是缺血性脑卒中的独立危险因素,应该重视CVR在脑缺血发生、发展过程中的独立影响作用。     

抽动症患者感觉运动整合的异常

抽动症的发病机制尚不十分明确,简单/复杂的感觉现象可能在抽动的发生中起到重要作用.越来越多的研究使用经颅磁刺激（TMS）等方法,探究抽动症患者经皮质环路输入与传出相互影响的机制,从不同角度证实了抽动症患者感觉运动整合的异常.     

原发性痉挛性斜颈感觉运动整合的研究进展

肌张力障碍是一种不自主、持续性肌肉收缩引起的扭曲、重复运动或姿势异常的综合征,其病理生理机制尚不明确。根据其症状分布,可以分为：局灶型、节段型、多灶型、全身型和偏身型。痉挛性斜颈（spasmodic torticollis）是成人发病的局灶性肌张力障碍中最常见的一种,可表现为头颈部不自主的扭转、侧倾、前屈和后仰,常伴有姿势性震颤及相应肌肉的痉挛性疼痛,通常可累及胸锁乳突肌、头夹肌、     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

Targeting 13-secretase with RNAi in neural stem cells for Alzheimer＇s disease therapy

There are several major pathological changes in Alzheimer＇s disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 （BACE1） and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein （AI3） production, and introduced it into the pSilenCircle vector to construct a short hairpin （shRNA） expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer＇s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

血浆谷胱甘肽过氧化物酶研究进展

谷胱甘肽过氧化物酶（glutathione peroxidases,GPX）是在哺乳动物中发现的,可通过还原性谷胱甘肽催化还原过氧化物和有机过氧化氢物,从而保护细胞和其他如DNA、蛋白及脂质体等敏感生物分子免受氧自由基的损伤。血浆谷胱甘肽过氧化物酶（GPx-3）是1987年Takahashi等从人的血浆中纯化得到的,是目前已知的GPX家族8个成员中唯一的细胞外亚型。研究发现有多种因素影响GPx-3的表达,并参与了多种疾病的发生、发展,本文就GPx-3的结构、功能、基因表达及其与疾病的关系作一综述。