慢性酒精中毒合并神经系统损害患者的脑电图和脑脊液改变

目的　探讨慢性酒精中毒合并神经系统损害患者的脑电图和脑脊液改变 ,以加强对慢性酒精中毒患者的防治提供依据。方法　对 4 2例慢性酒精中毒合并神经系统损害患者 (脑病 7例、脑病合并神经肌肉病 2 9例、周围神经病肌病 6例 )进行脑电图及腰穿脑脊液 (压力、常规、生化、IgG指数及血脑屏障指数 )检查 ,并以 30例长期大量饮酒但无中毒症状其它患者的脑电图作对照。结果　慢性酒精中毒患者的脑电图异常率76 19% ,明显高于对照组 19 2 % (P <0 0 0 1) ,且异常程度明显重于对照组 (P <0 0 0 1)。慢性酒精中毒患者的脑脊液压力、IgG指数、糖、氯化物均正常 ,但蛋白明显升高 ,2 8例患者血脑屏障有破坏。结论　慢性酒精中毒患者的神经系统损伤主要是长期酗酒致使营养不良以及酒精及其代谢产物的毒性作用造成血脑屏障损伤 ,而无明显的免疫损伤 ;脑电图异常可提示长期大量饮酒患者的神经系统损害 ,一旦发现应及时治疗。     

慢性酒精中毒伴癫(癎)发作临床特征分析

目的 探讨慢性酒精中毒伴癫(癎)发作患者的脑电图(EEG)及临床特征.方法 对28例慢性酒精中毒伴癫(癎)患者的EEG及临床资料进行回顾性分析.结果 EEG异常21例(75%),多表现为广泛轻中度异常,异常程度与临床神经精神症状的严重性相关,饮酒史越长,EEG异常越明显,且常有癫(癎)样放电.慢性酒精中毒可伴发癫(癎),癫(癎)发作多与突然戒酒及增减量有关.结论 EEG反映大脑功能状态,对慢性酒精中毒伴癫(癎)发作在诊疗、估计预后方面有积极作用.     

兔慢性酒精中毒性周围神经病动物模型的建立

目的慢性酒精中毒性周围神经病(PNCA)为酒精中毒常见的神经系统并发症之一.有必要探讨适合的慢性酒精中毒性周围神经病的动物模型.方法25只健康成年日本大耳兔随机分为2组,白酒灌胃组和对照组,白酒灌胃组给予56%(v/v)白酒按6 mL·kg-1·d-1灌胃;对照组用等体积生理盐水灌胃.每只家兔每月称体重,24周后进行肌电图检查,并作坐骨神经活检.结果(1)白酒灌胃组家兔的体重及食量较对照组差,并出现酒精中毒性精神症状.(2)电生理检查白酒灌胃组家兔均出现复合肌肉动作电位(CAMP)波幅降低,伴轻中度运动神经传导速度(MCV)减慢.(3)白酒灌胃组家兔HE染色与神经纤维GleeMarsland银染色光镜下均显示轴索变性伴继发节段性脱髓鞘改变.结论高浓度白酒灌胃24周,兔周围神经肌电图与病理改变均符合轴索性周围神经病变,这种改变与人类慢性酒精中毒性周围神经病相似.高浓度白酒灌胃制作兔PNCA动物模型是可行的.     

慢性酒精中毒性肌病的临床与神经电生理学研究

目的　探讨慢性酒精中毒性肌病的临床和电生理改变特点。方法　对 2 6例慢性酒精中毒性肌病、13例慢性酒精中毒性周围神经病、2 1例慢性酒精中毒性神经和肌肉混合损害患者 ,以及 2 0例正常受试者进行详细询问病史、查体 ,并记录酒精摄入量和测定相关神经电生理指标 ,包括肌电图、单纤维肌电图、肌纤维传导速度、周围神经传导速度和诱发电位。结果　 (1)酒精中毒性肌病的主要临床表现为肢带肌的无力、肌肉疼痛和萎缩 ,肌病的症状和体征往往先于周围神经的损害。 (2 )与正常对照受试者比较 ,各组患者神经肌肉颤抖值均增大 (t检验 ,P<0 .0 5 ) ,纤维密度增加 (t检验 ,P<0 .0 5 ) ,周围神经病组患者的神经肌肉颤抖值和纤维密度改变尤为显著 (t检验 ,P<0 .0 1)。 (3)肌病组患者肌纤维传导速度明显减慢 (t检验 ,P<0 .0 5 ) ,其余两组患者无显著变化 (t检验 ,P>0 .0 5 )。结论　 (1)酒精中毒性肌病临床主要表现为对称性肢带肌萎缩、肌力减退和肌肉疼痛。 (2 )肌电图提示肌源性改变 ,特别是肌纤维传导速度减慢 ,是诊断酒精中毒性肌肉病变的客观指征。     

慢性酒精中毒性神经病38例临床分析

慢性酒精中毒性神经病(CAND)是由于长期大量饮酒引起的营养代谢障碍及其代谢产物对神经系统的直接毒害作用.现将我院近6年来收治38例患者总结如下.     

慢性酒精中毒神经系统损害的临床分析

目的探讨慢性酒精中毒的临床表现类型、诊断与治疗。方法对43例慢性酒精中毒神经系统损害病人的临床表现、诊断与治疗效果进行分析。结果 慢性酒精中毒性神经系统损害多发生于饮用高度白酒半年以上,酒量>250ml/d者。其中大脑损害者居首位,继发小脑变性者次之,周围神经损害发生率较低。结论戒酒与早期诊治是治疗关键。有长期饮高度酒史,不能以其他疾病解释的精神症状,特别人格改变应考虑慢性酒精中毒性神经损害诊断。     

慢性酒精中毒患者的脑电图分析

酒精对脑组织有较大的亲和力 ,慢性酒精中毒对神经系统的影响越来越受到重视。现将我院 1998～ 2 0 0 3年对 60例慢性酒精中毒患者的脑电图 (EEG)分析报告如下。1　资料与方法1 1　一般资料　 60例患者均为男性 ,年龄 2 6～ 61岁 ,平均(3 2 3± 9 6)岁。诊断均符合CCMD -II -R中慢性酒精中毒的诊断标准〔1〕。发病年龄 2 2～ 5 7岁 ,病程 3个月至 4年 ,初饮酒年龄 12～ 42岁 ,平均 (2 3 8± 5 3 )岁 ,饮酒年限 6～ 3 3年 ,平均(15± 7 2 )年 ,均每日以晨饮、睡饮为主 ,日均饮酒量为 2 0 0～5 0 0ml不等 ,酒为低～高度白酒。1 2　神经…     

酒精和中枢神经系统

乙醇是全世界常用的神经毒药物之一,是一个严重影响健康的问题。本文将讨论慢性酒精中毒所致的神经系统合并症及其他一些有关问题。韦尼克—科萨科夫(Wernicke-Korsakoff Syn-drome,WKS)综合征。此综合征是硫胺缺乏引起的营养性神经系统疾患。韦尼克氏脑病代表其急性     

慢性酒精中毒患者血清中tau蛋白、Aβ1-42的测定及临床意义

目的研究酒精中毒患者血清tau蛋白及Aβ1-42测定的临床意义及其参与酒精致神经系统损害的机制。方法 40名慢性酒精中毒患者(饮酒时间均超过5年)按饮酒年限分为饮酒20年以上组及20年以下组。按头部CT结果分为脑萎缩组及无脑萎缩组。用ELISA方法测定40名酒精中毒患者及16名健康人的血清tau蛋白及Aβ1-42水平。结果 (1)慢性酒精中毒患者血清tau蛋白高于正常对照组,但两者之间无统计学意义。脑萎缩组血清tau蛋白水平显著高于无脑萎缩组及正常对照组,差异具有统计学意义(P<0.05)。饮酒20年以上组血清tau蛋白显著高于饮酒20年以下组以及正常对照组,差异有统计学意义(P<0.05)。(2)慢性酒精中毒患者血清Aβ1-42明显高于正常对照组,有统计学意义(P<0.01)。脑萎缩组及无脑萎缩组血清Aβ1-42均明显高于正常对照组,且有统计学意义(P<0.01)。饮酒20年以上组及饮酒20年以下组血清Aβ1-42均明显高于正常对照组,且有统计学意义(P<0.01)。结论 (1)慢性酒精中毒患者血清tau蛋白、Aβ1-42增高,可能对慢性酒精中毒的诊断有意义。(2)tau蛋白、Aβ1-42可能参与酒精致神经系统损害的机制。     

痉挛与神经系统重塑关系的研究

正痉挛是一种中枢神经系统损伤后异常的神经重塑(neuronal plasticity)的临床表现。本文就痉挛的发生与神经系统重塑之间的关系综述如下。一、痉挛的发生与神经系统重塑1.痉挛的产生痉挛(spasticity)是一种异常中枢神经系统的重塑性适应(plastic adaptation)现象~([1])。经典的Brunnstrom分期描     

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.     

Disrupted structural and functional brain connectomes in mild cognitive impairment and Alzheimer＇s disease

Alzheimer＇s disease （AD） is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging （structural magnetic resonance imaging （MRI）, diffusion MRI, and functional MRI） and neurophysiological techniques （electroencephalography and magnetoencephaJography） with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment （MCI）, the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks （i.e., connectomics） and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this 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。     

Correlation of hypoxia-inducible factor-1 alpha and erythropoietin protein and mRNA to cerebral ischemic tolerance in a focal ischemia/reperfusion model using the twice suture method

BACKGROUND： Numerous studies have shown that transient ischemic preconditioning induces cerebral ischemic tolerance. However, the underlying mechanisms of endogenous protection following ischemic preconditioning remain unclear. OBJECTIVE： To dynamically measure erythropoietin and hypoxia-inducible factor-1α （HIF-1α） mRNA and protein expression at various times following preconditioning, and to investigate effects of erythropoietin and HIF-1α on cerebral ischemic tolerance in a model of focal ischemia/reperfusion established using the twice suture method. DESIGN, TIME AND SETTING： The randomized, controlled study was performed at the Institute of Anatomy, Medical College, Qingdao University, China from March 2006 to March 2007. MATERIALS： Rabbit anti-rat HIF-1α monoclonal antibody and biotinylated goat anti-rabbit IgG （Boster, China）, rabbit anti-rat erythropoietin monoclonal antibody （Santa Cruz Biotechnology, USA）, and one-step RT-PCR kit （Qiagen, Germany） were used in this study. METHODS： A total of 99 healthy, male, Wistar rats were randomly assigned to three groups： sham surgery （n = 9）, non-ischemic preconditioning （n = 45）, and ischemic preconditioning （n = 45）. In the ischemic preconditioning group, rat models of pre-ischemia-reperfusion-ischemia-reperfusion were established by occluding the left middle cerebral artery using the twice suture method. In the non-ischemic preconditioning group, pre-ischemia was replaced by sham surgery. Subsequently, the ischemic preconditioning and non-ischemic preconditioning groups were equally divided into five subgroups according to time of first reperfusion, including 1-, 3-, 7-, 14-, and 21-day subgroups. The sham surgery group received the sham surgery twice. MAIN OUTCOME MEASURES： HIF-la and erythropoietin protein expression was measured in the cerebral cortex, corpus striatum, and hippocampus of the ischemic hemisphere. HIF-1α and erythropoietin mRNA expression were determined in the frontal and parietal cortex of the ischemic hemisphere. RESULTS： （1） Intergroup comparison： compared with the non-ischemic preconditioning group, HIF-1α protein expression significantly increased in the rat cerebral cortex, corpus striatum, and hippocampus in the ischemic hemisphere at 1,3, and 7 days following reperfusion in the ischemic preconditioning group （P 〈 0.05 or P 〈 0.01）. Erythropoietin protein expression significantly increased in the cerebral cortex, corpus striatum, and hippocampus, as well as HIF-1α and erythropoietin mRNA expression in the frontal and parietal cortex in the ischemic hemisphere, at 3 and 7 days following reperfusion in the ischemic preconditioning group （P 〈 0.05）. （2） Temporal expression： HIF-1α protein expression in the rat cerebral cortex, corpus striatum, and hippocampus, as well as HIF-la mRNA expression in the frontal and parietal cortex, in the ischemic hemisphere increased at 3 days, and gradually decreased from 7 days following reperfusion in the ischemic preconditioning group. Temporal erythropoietin protein and mRNA expression was consistent with HIF-1α protein expression. （3） Correlation： erythropoietin mRNA expression positively correlated with HIF-1α mRNA expression （r= 0.737, P 〈 0.01）. CONCLUSION： Ischemic preconditioning induced cerebral ischemic tolerance. Pre-ischemiainduced increase in endogenous HIF-1αexpression, as well as its target gene erythropoietin, participated in the formation of cerebral ischemic tolerance.     

雷公藤内酯对癫痫大鼠神经元P13K／Akt／mTOR蛋白的影响

目的通过检测癫痫大鼠海马神经元P13K、Akt和mTOR蛋白表达,探讨雷公藤内酯抑制癫痫大鼠神经元凋亡的分子机制。方法30只大鼠随机分为对照组、海人酸组、雷公藤内酯干预组,免疫组化法检测各组大鼠海马神经元P13K、Akt和mTOR蛋白的表达情况。结果海人酸组神经元胞体皱缩,形态不规则,数量减少,而雷公藤内酯干预组神经元的数量和形态与对照组相似,海人酸组海马神经元P13K、Akt、ITITOR蛋白表达与对照组比较均减少,而雷公藤内酯干预组海马神经元的P13K、Akt、mTOR蛋白表达均较海人酸组增加,差异均有统计学意义（P〈0．05）。结论雷公藤内酯可能通过上调P13K／Akt／mTOR信号通路蛋白表达对癫痫大鼠海马神经元发挥保护作用。     

Dysfunctional autophagy in Alzheimer＇s disease： pathogenic roles and therapeutic implications

Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer＇s disease （AD）. The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.     

Oxidative stress in Alzheimer＇s disease

Oxidative stress plays a significant role in the pathogenesis of Alzheimer＇s disease （AD）, a devastating disease of the elderly. The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons （lipids, proteins, and nucleic acids） can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, inflammation, and β-amyloid （Aβ） peptides. Oxidative stress participates in the development of AD by promoting Aβ deposition, tau hyperphosphorylation, and the subsequent loss of synapses and neurons. The relationship between oxidative stress and AD suggests that oxidative stress is an essential part of the pathological process, and antioxidants may be useful for AD treatment.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

乙醇脱氢酶1C多态性与酒精依赖及相关疾病的研究进展

乙醇脱氢酶(Alcohol Dehydrogenase,ADH)1C是目前受到广泛关注的ADH同工酶,其遗传多态性影响酒精依赖的发生、发展.在不同地域,不同人种间,对ADH1C多态性与酒精依赖的研究结果存在较大的差异,现就ADH1C遗传多态性与酒精依赖及饮酒相关心血管、消化系统和女性特有疾患的关系进行综述,探讨其对酒精依赖及与饮酒相关疾病的影响.