症状严重程度比认知缺损更与精神分裂症住院患者的社会功能状况密切相关(英文)

背景以往研究表明精神分裂症患者的神经认知缺损和精神病性症状会导致其职业和社会功能降低。目的评估中国精神分裂症男性住院患者的神经认知和精神病性症状与社会心理功能之间的关系。方法选取上海市精神卫生中心的51例住院男性精神分裂症患者,其中40例患者最终完成了个体和社会功能量表(Personal and Social Performance Scale,PSP)中文版、临床疗效总评量表-病情严重程度量表(Clinical Global Impression-Severity,CGI-S)、阳性和阴性症状量表(Positive and Negative Symptom Scale,PANSS)、字母-数字排序以及香港文字记忆学习测试等项目的评定。结果患者PANSS量表的3个临床分量表的分值和社会功能总体评估(PSP总分和CGI-S分值)之间存在明显负相关。患者的神经认知测定结果与症状或社会功能状况均无关。结论对于急性期住院精神分裂症患者而言,临床症状的严重度—而非神经认知缺损程度,与其社会功能水平密切相关。     

精神分裂症患者认知功能损伤的研究进展

为进一步了解精神分裂症神经生物学机制并为未来的相关研究及诊疗提供新思路,故对精神分裂症认知功能损伤的研究进行综述。认知功能受损是精神分裂症的重要临床表现之一。目前使用蒙特利尔认知评估量表(MoCA)及精神分裂症认知功能成套测验共识版(MCCB)评定精神分裂症患者的认知功能均发现患者存在严重的工作记忆障碍。工作记忆是大脑前额叶皮质的主要功能之一,而纹状体突触前合成和分泌的多巴胺(DA)含量与认知功能损伤程度及前额叶皮质功能存在相关性。对认知功能损伤的治疗有助于改善精神分裂症患者的预后、减轻社会负担。目前已有多种治疗方式可供选择。     

精神分裂症患者认知功能与社会功能的相关性

目的探讨精神分裂症恢复期患者认知功能对社会功能的影响。方法对80例精神分裂症恢复期患者采用瑞文标准测验（CRT）、韦氏成人智力量表（WAIS）、威斯康星卡片测验（WCST）,分别与社会功能缺陷量表（SDSS）进行多重线性回归分析。结果经逐步回归分析显示,WCST中变量（正确反应数、持续错误数、分类数）、WAIS中言语量表分、CRT中瑞文总分进入回归方程,拟合的回归方程均有统计学意义。其中瑞文总分、言语量表分与SDSS呈线性负相关关系,持续错误数与SDSS呈线性正相关关系;比较WCST、CRT、WAIS与SDSS的相关性,回归模型的拟合最好的为WCST。结论精神分裂症患者的认知功能与社会功能有显著相关性,正确的评测及改善认知功能对提高患者的社会功能有重要意义,WCST提供了一个有效预测精神分裂症患者社会功能的重要方法。     

利培酮维持治疗精神分裂症3年疗效观察

目的探讨利培酮治疗精神分裂症的长期疗效、安全性及其对认知功能的影响。方法92 例利培酮治疗的精神分裂症患者完成为期3年的观察,采用了阴性和阳性症状量表(PANSS)、简明精神病评定量表(BPRS)、副反应量表(TESS)、简易精神状态检查量表(MMSE)评定药物治疗的疗效与安全性及其对认知功能的影响。结果利培酮维持治疗期间,BPRS持续下降,疗效好,副作用少,不影响患者认知功能。结论利培酮治疗精神分裂症远期疗效稳定,安全性高,有利于患者重返社会。     

奥氮平和氯氮平对慢性精神分裂症的认知功能的影响

目的了解奥氮平和氯氮平对慢性精神分裂症患者的认知功能的影响。方法78例经典型抗精神病药物治疗疗效不显著或不能耐受不良反应的慢性精神分裂症患者随机替换为奥氮平及氯氮平治疗,分别在入组前、12周、6个月进行PANSS量表评定、认知功能测定,包括言语学习、记忆、注意、执行功能、精神运动。结果奥氮平组32例和氯氮平组34例完成了6个月的治疗,这些患者疗程结束时均显示精神症状显著改善,认知功能显著提高,表现为言语流畅性、言语学习、言语视觉记忆、执行功能方面。二者之间无显著差异。结论奥氮平和氯氮平均可改善慢性精神分裂症的认知功能,且二者的疗效相似。     

双益平对精神分裂症患者认知功能影响的对照研究

目的观察双益平对精神分裂症患者认知功能的影响。方法将76例诊断为精神分裂症的患者随机分成2组,其中一组(n=36)给予双益平治疗；另一组(n=40)为对照组,治疗8周,在入组前、治疗8周末分别进行韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)及副反应量表(TESS)评分,比较双益平组对精神分裂症患者认知功能产生的影响。结果两组8周后,双益平组认知功能的改善与对照组比较差异有显著性。结论双益平能改善精神分裂症患者的认知功能,其中尤以对记忆的改善为突出。     

开放式管理并认知行为治疗对慢性精神分裂症康复的对照研究

目的探讨开放式管理合并认知行为治疗对慢性精神分裂症患者的康复效果。方法试验组38例慢性精神分裂症患者在药物治疗的基础上,采用开放式管理合并认知行为治疗进行系统的康复治疗,对照组31例慢性精神分裂症患者采用传统西药治疗,两组在治疗前、6个月末及9个月末用社会功能缺陷筛选量表(SDSS)、日常生活能力量表(ADL)及阴性症状量表(SANS)观察疗效。结果康复训练9个月后,SDSS量表评分、ADL量表评分、SANS量表评分与对照组差别显著。结论开放式管理合并认知行为治疗对慢性精神分裂症病人康复疗效肯定,是慢性精神分裂症病人回归社会的有效途径。     

精神分裂症患者认知功能与服药依从性的相关性

目的 探讨精神分裂症患者的认知功能与服药依从性的关系.方法 采用便利抽样法,选取于2020年9月～2020年12月在湖南省某医院就诊的87名精神分裂症患者进行调查,主要包括一般情况调查表、药物依从性评定量表、精神分裂症简明认知功能成套测评量表和自知力与治疗态度问卷.结果 Pearson单因素分析显示,认知测评中符号编码...     

MCCB测定首发精神分裂症患者及其生物学父母存在认知功能障碍（英文）

背景:精神分裂症的临床表现为特征性的知觉、思维、情感和行为等障碍。认知障碍也是精神分裂症核心症状之一。20世纪70年代早期Gallhofer曾提出过,精神分裂症除有阳性或阴性症状,也存在认知障碍。许多研究表明,精神分裂症的一级亲属中存在遗传易感性。认知障碍不仅急性期存在,维持巩固期也会有。有研究还显示,精神分裂症健康的一级亲属亦存在认知缺陷。但对精神分裂症及其生物学父母的认知特征研究仍缺乏。本研究,我们假设精神分裂症及其生物学父母存在特定的认知功能障碍,拟采用认知功能成套测验共识版(MATRICS Consensus Cognitive Battery,MCCB)中文版,以探讨精神分裂症患者及其生物学父母的认知模式。目的:精神分裂症的认知特征可能受到其生物学父母认知模式的影响。研究旨在描绘精神分裂症患者与其父母之间的功能失调的认知模式。方法:采用认知功能成套测验共识版(MCCB,一种新的测量工具)评估29例首发精神分裂症(符合ICD-10精神分裂症诊断标准,年龄17-45岁),58例精神分裂症患者的生物学父母(年龄40-70岁)和46例健康对照(年龄40-70岁)的认知功能,以探讨精神分裂症患者及其生物学父母之间的认知功能障碍之间的关系。所有数据使用SPSS18.0统计软件进行分析。结果:1)男性精神分裂症患者与其父亲相比在MCCB认知功能测定的6个维度有明显认知缺陷(除社会认知功能外)。女性患者的工作记忆和问题推理能力都低于其母亲。2)患者父亲和健康对照组之间的工作记忆和推理问题也存在显著差异。3)与健康对照组相比,患者母亲在问题推理方面没有明显的差异,但视觉记忆有异常。结论:首发精神分裂症患者及其生物学父母在6个维度存在认知功能障碍。患者父母在工作记忆、问题推理和视觉记忆等方面也存在明显功能障碍。仍需深入研究以揭示首发精神分裂症及其生物学父母存在认知功能障碍的潜在机制。     

奥氮平对首发精神分裂症患者的疗效及认知功能影响

目的观察奥氮平对首发精神分裂症患者的疗效及认知功能的影响。方法对31例首发精神分裂症患者在奥氮平治疗前及治疗12周后，用阳性症状量表（SAPS）、阴性症状量表（SANS）、韦氏成人智力量表（WAIS—R）、韦氏记忆量表（WMS）、简明精神病评定量表（BPRS）、韦斯康星卡片分类测验（WCST）进行评估，并观察奥氮平对精神分裂症症状的疗效及对认知功能的影响。结果治疗后SAPS、SANS、BPRS〈WCST中错误应答数的评估分值显著降低（P〈0．01），且非持续性错误、WMS的再生、理解评估分值也明显降低（P〈0．05）。结论奥氮平治疗精神分裂症疗效可靠并可显著改善部分患者的认知功能。     

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.     

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.     

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.     

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。     

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.     

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.     

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.