癫痫伴抑郁筛查和治疗研究现状

正抑郁是癫痫患者伴发精神疾病当中最普遍的一种,大约累及1/3的癫痫患者[1]。癫痫和抑郁之间存在紧密的相互联系,可能拥有一些共同的发病机制[2]。在癫痫患者身上,抑郁经常被低估以及管理不足。有研究显示,抑郁会严重干扰癫痫的治疗效果以及损害癫痫患者的生活质量;同时,对抑郁的管理不足也被认为与癫痫患者的职业倦怠程度、医疗卫生使用率、医疗费用呈显著正相关[3]。因此,对癫痫患者而言,抑郁的早期发现和恰当管理显得尤     

癫痫间与抑郁共存75例临床分析

癫痫间是由于脑内神经元过度同步异常放电所致,其特点是具有发作性、暂时性的中枢神经系统功能失调。抑郁也是由于大脑皮层功能障碍所致。临床工作中发现癫痫间患者常合并抑郁,癫痫间和抑郁两者之间具有共存及相关性倾向,如患者存在一个疾病因素(癫痫间/抑郁)时,极其容易促发另外一个疾病(抑郁/癫痫间)发病。现报道2005年6月～2010年6月癫痫间门诊就诊的75例癫痫间合并抑郁患者如下,探讨其临床特点及两者之间的关系。     

应激与癫痫和抑郁相关性研究进展

癫痫和抑郁都是神经科常见病。两者在许多患者中共同存在绝非偶然。抑郁症患者比正常人有更高的癫痫患病率,癫痫患者抑郁症状的产生也不能仅仅归咎于单纯的社会心理因素。抑郁症和癫痫之间可能存在某种生物学联系,这种联系构成两者共病的基础。其中应激引起的海马萎缩、神经可塑性改变及神经再生受抑制是其重要原因。加强这方面的研究,将有利于揭示两者的发病机制、改善治疗效果、提高患者生活质量。     

癫(痫)与抑郁共存75例临床分析

癫痫间是由于脑内神经元过度同步异常放电所致,其特点是具有发作性、暂时性的中枢神经系统功能失调.抑郁也是由于大脑皮层功能障碍所致.临床工作中发现癫痫间患者常合并抑郁,癫痫间和抑郁两者之间具有共存及相关性倾向,如患者存在一个疾病因素(癫痫间/抑郁)时,极其容易促发另外一个疾病(抑郁/癫痫间)发病.现报道2005年6月~2010年6月癫痫间门诊就诊的75例癫痫间合并抑郁患者如下,探讨其临床特点及两者之间的关系.     

癫痫共病抑郁的机制及临床诊疗

本文目的是探讨癫痫共病抑郁的可能机制及临床诊疗。癫痫是一种常见的、慢性的、致残性的神经疾病,癫痫患者生活质量下降,存在明显的负性情绪,常伴发各种精神疾病。癫痫与抑郁具有共同的神经生物学基础,可能存在共同的发病机制。本文从癫痫共病抑郁的发病机制、临床诊断及治疗方面予以总结归纳。     

偏头痛与癫关系的临床观察

目的探讨偏头痛与癫痫的关系。方法收集偏头痛患者及癫痫患者病史、临床表现、脑电图等资料,进行回顾性分析。结果偏头痛组患者及癫痫组患者经对照研究分析,相对危险度（RR）值均位于95％置信区间内。结论偏头痛与癫痫存在双向联系,偏头痛可能是癫痫的病因或危险因素,癫痫也可能引起偏头痛样发作。     

癫痫伴发抑郁的研究进展

<正>近些年来,越来越多的研究致力于探究癫痫与情感障碍的关系,尤其是癫痫与抑郁的相互作用关系。癫痫是最常见的神经系统疾病之一,而抑郁障碍是癫痫最常见的伴发疾病之一。目前的研究表明,癫痫是抑郁的危险因素,原发抑郁更易于促发癫痫。并且,癫痫伴发抑郁较非抑郁癫痫个体相比,其治疗总体预后相对较差。癫痫与抑郁是共生关系,两者在病理生理上以及社会支持等方面共享某些机制。癫痫和抑郁在内分泌、神经递质、免疫以及颅内某些结构的异常方面表现出一致性。两者的相互影响关系表现在:一方面,严重的、难治性的、反复发作的癫痫更加容易伴发抑郁,抑郁能够加重癫痫的致残致死率,形成一种恶性循环;另一方面,     

癫痫患者个性研究

目的：探讨癫痫患者的个性特征。方法：采用艾森克个性问卷对１１４例癫痫患者进行个性测查。结果：癫痫患者有明显的个性异常,较孤僻,易攻击,报复心强,情绪控制能力差,残忍。发病年龄愈小,个性改变愈严重。结论：癫痫患者存在明显的个性异常。     

成人癫痫与抑郁

癫痫作为神经系统的常见慢性疾病已经成为一个全球健康问题,癫痫共患病的存在进一步恶化了癫痫的结局,加剧了不良社会后果。抑郁障碍是癫痫最常见共患病,并导致癫痫患者对抗癫痫药物的耐受性低、服药依从性低、治疗效果差、生活质量下降、认知障碍增加、其他慢性疾病和自杀的风险增加等一系列不良后果,进一步恶化了癫痫的结局。目前,癫痫共患抑郁存在着高发病率、低诊断率、低治疗率的现状,癫痫共患抑郁的筛查、评估和管理应成为癫痫临床不可或缺的组成部分。     

癫痫的精神病症状群

癫痫和精神疾病的密切关系长期以来是精神科领域中一个引人关注的问题,两个论点在不同时期主宰着精神科对两者联系的看法,一是两者互相对抗,一是两者在临床上同时存在。一、癲痫的短暂精神病性发作(一)意识模糊状态和非意识模糊状态持续数小时或数天精神和行为障碍长期以来被认为是癫痫的特征。上世纪欧洲学者认为这是一组特殊的精神病,并称之为“癫痫性躁狂症”“未成熟的癫痫”和“精神性大发作”,然而未考虑这些状态时意识模糊存在与否的意义。     

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.     

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.     

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.     

GluN2A versus GluN2B：twins,but quite different

N-Methyl-D-aspartate receptors（NMDARs） play vital roles in the central nervous system,as they are primary mediators of Ca2＋influx during synaptic activity.The subunits that compose NMDARs share similar topological structures but are distinct in distribution and pharmacological properties,as well as physiological and pathological functions,which make the NMDAR one of the most complex and elusive ionotropic glutamate receptors.In this review,we focus on GluN2A and GluN2B,the primary NMDAR subunits in the cortex and hippocampus,and discuss their differences in developmental expression,brain distribution,trafficking,and functional properties during neuronal activity.     

齐拉西酮与利培酮治疗精神分裂症的对照研究

目的 评价齐拉西酮治疗精神分裂症的疗效和安全性.方法 选择90例精神分裂症患者随机分为齐拉西酮组(139.6±23.5)mg/d和利培酮组(5.8±0.6)mg/d,疗程为8周.采用阳性与阴性症状量表(PANSS)、临床总体印象量表(CGI- S)和不良反应症状量表(TESS),分别于入组时(基线)、治疗后第2、4、6、8周末分别评定疗效和不良反应.结果 两组PANSS总分、阳性症状分、一般病理分从第2周末起较治疗前下降(P＜0.05);两组PANSS阴性症状分在第4周末起较治疗前下降(P＜0.05);两组CGI-S总分第2周末开始各时点较治疗前下降(P＜0.05);齐拉西酮组临床总有效率为75％,利培酮组为78.4％,两组间疗效差异无统计学意义(P＞0.05).齐拉西酮组、利培酮组不良反应发生率分别为26.6％(12/45)和51.1％(23/45),差异有统计学意义(P＜0.01);利培酮组体质量增加(1.1±1.3)kg,齐拉西酮组体质量减少(1.4±1.5)kg,在锥体外系有关的副反应、血细胞、肝功能、心电图异常及自主神经系统不良反应方面利培酮组明显高于齐拉西酮组,差异有统计学意义(P＜0.01).结论 齐拉西酮对精神分裂症的疗效等同于利培酮,而不良反应全面优于利培酮.     

Wnt信号通路与骨髓间充质干细胞增殖及分化的关系

骨髓间充质干细胞（bonemarrow—derived mesenchymal stem cells,BMSCs）是骨髓中不同于造血干细胞的一类细胞,其来源丰富,取材简便,易分离、纯化、培养,在一定的条件下可以迅速体外扩增,具有多向分化潜能,可以通过不同的方法被诱导分化成骨细胞、软骨细胞、肌细胞、神经胶质细胞、神经元细胞等,而且它具有低免疫源性,向病变部位迁移的能力,     

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.     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。     

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。     

焦虑与心血管疾病的相关性分析

近年来,我国所患心血管疾病的人口比例越来越高,而焦虑症作为伴发心血管疾病的常见性疾病,对其识别与否以及处理的是否得当将对心血管疾病的预后产生重大影响,但目前国内外对此的研究还相对欠缺,现对此做一综述,综合相关文献,对此方面的问题进行研究。