无抽搐电休克治疗对精神分裂症的效果及患者认知功能的影响

目的探讨无抽搐电休克治疗(MECT)对精神分裂症的效果和患者认知功能的影响。方法将符合《国际疾病分类(第10版)》(ICD-10)精神分裂症诊断标准的50例精神分裂症患者作为研究组,进行为期6周的MECT治疗;将50例在性别、年龄、病程、教育程度、诊断上相匹配的单纯药物治疗的患者作为对照组,在治疗前、治疗结束后1天和治疗后2周分别进行阳性与阴性症状量表(PANSS)、威斯康星卡片分类测验(WCST)和韦氏记忆测验(WMS)评定。结果治疗后1天和治疗后2周两组PANSS总评分和各项因子分均较治疗前低,差异有统计学意义(P0.01)。治疗后1天和治疗后2周研究组WCST的错误应答数和持续性错误数项目得分比治疗前和同期对照组低(P0.05)。治疗后研究组WMS的再认、图片和联想的项目得分比治疗前和同期对照组均低(P0.05)。治疗后研究组理解项目得分比治疗前和同期对照组高(P0.05)。结论合并MECT治疗能快速缓解急性期精神分裂症患者的阳性症状,对记忆可能有部分短暂而可逆的影响,而对执行功能有着不同程度的改善。     

无抽搐电休克对精神分裂症记忆、认知功能及脑电图的影响

目的研究无抽搐电休克疗法(Modified Electra convulsive Therapy,MECT)对精神分裂症患者的记忆、认知功能及脑电状况的影响。方法回顾性分析2012年5月～2017年10月我院收治的100例精神分裂症患者,将其分为观察组和对照组,每组各50例;对照组采用常规药物治疗,观察组在对照组基础之上配合无抽搐电休克治疗。治疗3月后评估两组的治疗效果、治疗后记忆能力、认知功能及脑电状况。结果观察组的治疗总有效率明显高于对照组,差异有统计学意义(P0.05);观察组患者治疗后的简易智能精神状况量表(MMSE)得分及蒙特利尔认知评估量表(MoCA)评分较对照组明显更高,差异具有统计学意义(P0.05);观察组患者的WMS评分较对照组更高,差异具有统计学意义(P0.05);观察组患者也更少发生脑电异常的状况,其间差异具有统计学意义(P0.05)。结论无抽搐电休克治疗对精神分裂症患者有着很显著的疗效,且能够有效改善患者的记忆能力、认知功能以及脑电状况,值得临床运用和推广。     

重复经颅磁刺激和无抽搐电休克对慢性精神分裂症阴性症状的疗效比较

目的:比较重复经颅磁刺激(rT MS)和无抽搐电休克治疗(MECT)对慢性精神分裂症患者阴性症状的疗效及安全性。方法:80例慢性精神分裂症住院患者分为rT MS组和MECT组,各40例。rT MS组接受rT MS治疗,MECT组接受MECT,观察4周。采用阳性和阴性症状量表(PANSS)、治疗中出现的症状量表(TESS)及韦氏记忆量表(WMS)在治疗前和治疗结束时评估症状及不良反应,比较两组疗效及安全性。结果:治疗4周,rT MS组PANSS总分、阳性症状、阴性症状及一般精神病理评分差值显著高于MECT组(F=11.890,F=14.406,F=17.850,F=37.682;P均0.05);WMS评分再认、图片、联想及背数记忆评分差值rT MS组显著低于MECT组(F=28.500,F=43.530,F=29.125,F=25.232;P均0.05);MECT组TESS评分显著高于rT MS组(F=46.805,P0.05)。结论:rT MS治疗较MECT更能在短期内改善精神分裂症患者阴性症状,且安全性更高。     

无抽搐电休克治疗对记忆及抽象思维的影响

目的:探讨无抽搐电休克治疗(MECT)对精神分裂症患者记忆功能及抽象思维能力的影响. 方法:对37例精神分裂症患者采用修订韦氏记忆测验(WMS)和韦氏智力测验中的木块图案分测验在治疗前后分别评定. 结果:治疗后患者图片、再认、再生、经历、联想和木块图案得分明显高于治疗前. 结论:MECT可能对精神分裂症患者的记忆功能和抽象思维能力不造成损害.     

无抽搐电休克维持治疗对难治性精神分裂症患者的疗效和认知功能的影响

目的:探讨无抽搐电休克维持治疗(M-ECT)对难治性精神分裂症患者的疗效和认知功能的影响。方法:将60例难治性精神分裂症患者随机分为两组,给予研究组药物联合为期26周的MECT,对照组仅使用药物治疗;治疗前、治疗2周、4周、13周和26周分别进行阳性与阴性症状量表(PANSS)、威斯康星卡片分类测验(WCST)、韦氏记忆测验(WMS)评定。结果:治疗后各时间点两组PANSS总分、治疗2周后的阳性症状分、治疗4周后的阴性症状分和一般病理分均较基线时明显下降(P均0.05);研究组PANSS总分在治疗13周、26周明显低于对照组(P均0.05);阳性症状分治疗后各时间点明显低于对照组(P均0.05);阴性症状分和一般病理分在治疗26周明显低于对照组(P均0.05)。治疗13周时,WCST完成分类数、WMS联想得分明显高于对照组(P均0.05);治疗26周时,WCST错误应答数明显低于对照组;WMS再认、联想得分明显高于对照组(P均0.05)。结论:药物联合M-ECT能快速缓解难治性精神分裂症患者的阳性症状,疗效优于单纯药物治疗,并对患者部分记忆和执行功能有改善。     

无抽搐电休克治疗难治性精神分裂症临床观察

目的:了解无抽搐电休克治疗(MECT)对难治性精神分裂症的疗效与不良反应。方法:对39例难治性精神分裂症患者在原服用抗精神病药基础上合并MECT治疗,分别于合并治疗前后采用阳性与阴性症状量表(PANSS)及副反应量表(TESS),韦氏记忆量表(WMS)评定疗效及不良反应。结果:合并MECT后PANSS评分明显降低(P<0.01),WMS评分在治疗结束后1d明显降低,1周及2周时恢复。结论:MECT对难治性精神分裂症有效,不良反应少。     

不同疗程无抽搐电休克治疗难治性精神分裂症的对照研究

目的比较不同疗程无抽搐电休克治疗（EMCT）对难治性精神分裂症TRS的疗效与副反应。方法将102例难治性精神分裂症患者随机分为两组,一组给予12次MECT治疗（实验组n=52）,另一组给予8次MECT治疗（对照组n=50）;观察两组样本的有效率、阳性与阴性症状量表（PANSS）总分、治疗相关症状量表（TESS）总分、韦克斯勒记忆量表（WMS）总分变化。结果两组有效率在MECT治疗4次末、8次末、12次未表现出统计学差异（P均＞0.05）,各组组内前后比较也未表现出统计学差异（P均＞0.05）;PANSS总分在各测量时点组间差异不显著（P均＞0.05）,但第4次、8次、12次评分与入院时相比差异有统计学意义（P均＜0.05）;TESS总分各时点测量组间差异无显著性,但在第8次时与入组时比较差异具显著性（P＜0.01）;WMS各测量时点组间及各组与入组时比较均无显著性意义（P均＞0.05）。结论不同疗程MECT对TRS的短期疗效、副反应的影响无差别;MECT对TRS有效、安全;应当进一步研究MECT的作用机制。     

无抽搐电休克对抑郁症记忆功能及抽象思维能力的影响

目的初步探讨无抽搐电休克治疗(MECT)对抑郁症患者的记忆功能及抽象思维能力的影响.方法对19名抑郁症患者采用修订韦氏成套记忆测验(WMS)、木块图和第四例外测验对19例抑郁症患者在治疗前、治疗后第一个24 h以及所有治疗终止后第一个24 h共三个时间段进行重复测验. 结果三个时间段的记忆商数差异均无显著性(P＞0.05);"联想"和"木块图"得分在三个不同时间段的得分差异有显著性(P＜0.05),治疗后得分明显高于治疗前. 结论无抽搐电休克可能对抑郁症的记忆功能和抽象思维能力不造成影响.     

无抽搐电休克与氟哌啶醇针剂治疗急性期精神分裂症的对照研究

目的比较无抽搐电休克(MECT)与氟哌啶醇针剂对急性期精神分裂症的疗效和安全性。方法采用数字随机法将90例急性期精神分裂症患者分成MECT组和氟哌啶醇组,疗程为1周,分别在治疗前、治疗后1、3和7天末采用阳性与阴性症状量表(PANSS)评定疗效,用副反应量表(TESS)和韦氏记忆量表(WMS)评定不良反应。结果治疗结束后,MECT组显效率为59.10%,有效率90.90%;氟哌啶醇组显效率为55.80%,有效率88.40%,两组间差异无统计学意义(P>0.05)。治疗后两组患者的PANSS总分和阳性症状因子分较治疗前均降低(P<0.05),在治疗后第3天和第7天末MECT组的PANSS总分和阳性症状因子分均低于氟哌啶醇组(P<0.05)。治疗结束时MECT组WMS总分较治疗前降低(P<0.05),但至2周已完全恢复到治疗前水平(P>0.05)。不良反应发生率,MECT组低于氟哌啶醇组,两组差异有统计学意义(P<0.01)。结论 MECT对急性期精神分裂症的治疗是有效而安全的,值得在临床中应用。     

阿尼西坦改善慢性精神分裂症患者认知功能的临床研究

目的探讨阿尼西坦改善慢性精神分裂症患者认知功能的疗效。方法将64例慢性精神分裂症患者随机分为研究组32例和治疗组32例,分别予以奎的平(350±50)mg/d治疗8周,研究组同时合并阿尼西坦100mg/d,并于治疗前及治疗后分别进行阳性和阴性症状量表(PANSS)、简明精神状态量表(MMSE)、中国修订韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)及威斯康星卡片分类测定(WCST)等评定,并与正常人组成的对照组进行比较。结果治疗前研究组和治疗组的MMSE、WMS及WAIS-RC均低于对照组,差异有显著性(P〈0.05),提示患者的认知功能有广泛性损害。治疗后研究组MMSE、WCST、WMS、WAIS-RC分数与治疗前比较差异有显著性(P〈0.05),而治疗后治疗组的WCST、WMS、WAIS-RC分数与治疗前比较无显著性差异(P〈0.05)。结论阿尼西坦改善慢性精神分裂症患者的认知功能疗效确切。     

双额侧或双颞侧无抽搐电休克疗法对难治性精神分裂症疗效及记忆功能的影响

目的探讨电极放置位置对无抽搐电休克治疗疗效及对记忆功能影响。方法选择符合入组标准的难治性精神分裂症患者60例,随机分为双额侧组和双颞侧组,各30例,疗效测定使用PANSS量表,于治疗前、治疗第1、4、8、12次后分别测定,记忆功能测定使用wMS量表,分别于治疗前及疗程结束后进行测定。结果治疗前两组PANSS及wMs各项指标差异无统计学意义,第1次治疗后双额侧组PANSS阳性症状及总分开始改善（P〈0．05）,双颞侧组在第4次治疗后才出现改善（P〈0．05）;两组组间比较,第4周两组间阳性症状、阴性症状、总分差异有统计学意义（P〈0．05）;疗程结束后两组间PANSS指标及有效率差异无统计学意义（P〉0．05）。WMS量表显示双额侧组明显比双颞侧带来的记忆功能影响小。结论双额侧电极放置MECT治疗难治性精神分裂症相对双颞侧起效快,疗效相当,对记忆功能影响程度小。     

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.     

不同的电极放置方式对无抽搐电休克治疗抑郁症的疗效及认知功能的影响

目的 探讨不同的治疗电极放置方式对无抽搐电休克治疗抑郁症的疗效及认知功能的影响.方法 将100例抑郁症患者随机分成两组,每组各50例,分别实施双侧电极（双颞侧）与单侧电极（非优势侧大脑顶颞部）无抽搐电休克治疗.采用汉密尔顿抑郁量表（HAMD）、修订韦氏成套记忆测验（WMS）、木块图和第四例外测验分别评定两组的疗效和认知功能. 结果两组患者的总体疗效相当,但对认知功能的影响存在差异,双侧电极对认知功能有影响,但2周内可恢复.结论 单、双侧电极放置对抑郁症疗效相当,单侧电极对认知功能无影响,双侧电极对认知功能有影响但可恢复.     

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。     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

Aging effects of regional activation in a spatial task A functional magnetic resonance imaging study

BACKGROUND： An increasing number of studies have shown the effects of aging in basic cognitive processing and higher cognitive functions using functional magnetic resonance imaging （fMRI）. However, little is known about the aging effects in diverse cognitive abilities, such as spatial learning and reasoning.
OBJECTIVE： To investigate the effect of aging on spatial cognitive performance and regional brain activation based on fMRI.
DESIGN, TIME, AND SETTING： A block design for fMRI observation. This study was performed at the fMRI Laboratory, Brain Science Research Center, Korea Advanced Institute of Science and Technology from March 2006 to May 2009.
PARTICIPANTS： Eight right-handed, male, college students in their 20s （mean age 21.5 years） and six right-handed, male, adults in their 40s （mean age 45.7 years）, who graduated from college, participated in the study. All subjects were healthy and had no prior history of psychiatric or neurological disorders.
METHODS： A spatial task was presented while brain images were acquired using a 3T fMRI system （ISOL Technology, Korea）. The spatial tasks involved selecting a shape that corresponded to a given figure using four examples, as well as selecting a development figure of a diagram.
MAIN OUTCOME MEASURES： The accuracy rate （number of correct answers/total number of items x 100%） of spatial tasks was calculated. Using the subtraction procedure, the activated areas in the brain during spatial tasks were color-coded by T-score. The double subtraction method was used to analyze the effect of aging between the two age groups （20s versus 40s）.
RESULTS： The cerebellum, occipital lobe, parietal lobe, and frontal lobe were similarly activated in the two age groups. Increased brain activations, however, were observed in bilateral parietal and superior frontal lobes of the younger group. More activation was observed in bilateral middle frontal and right inferior frontal lobes in the older group. Compared with the older group, the younger men exhibited greater spatial performance （P = 0.012）.
CONCLUSION： Reduced cognitive function correlated with decreased activation areas in the parietal lobe and altered activation in the frontal lobe.     

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.     

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.