住院森田疗法治疗33例精神分裂症患者人格特征分析

目的 探讨住院森田疗法对精神分裂症患者人格特征的影响.方法 选择符合入组标准的住院精神分裂症病人66例,随机分为森田组,对照组,共冶疗10周,采用MMPI多相个性测查表（中国版本399题）分别于冶疗前后进行测查.结果 两组中Hs、Pt、Sc、Si量表T分变化组间比较有显著性差异.结论 森田疗法能矫正病人的某些病态人格.     

精神分裂症患者凶杀行为多因素分析

目的探讨精神分裂症患者凶杀行为的影响因素。方法应用人口学资料、阳性与阴性症状量表（PANSS）、明尼苏达多相人格调查表（MMPI）、生活事件量表（LES）和社会支持评定量表（SSRs）等对31例具有凶杀行为的精神分裂症患者和50例无凶杀行为的患者进行对照研究。结果两组的PANSS量表阳性症状量表分、阴性症状量表分、MMPI的D（抑郁）、Hy（癔病）、Pd（人格偏移）,Mf（男性化和女性化）、Pa（偏执）、Pt（精神衰弱）、Sc（精神分裂症）、Si（社会内向性）量表分、负性事件刺激量、客观支持量表分等项目得分的差异,有统计学显著意义。多因素分析中,阴性症状,客观支持,D,Mf,Pt,sc进入回归方程。结论本研究提示负性事件、阴性症状、客观支持、D、Mf、Pt、Sc与精神分裂症患者凶杀行为有关联,可作为其预测因子。     

改良森田疗法对康复期精神病性障碍患者人格的影响

目的:观察改良森田疗法对康复期精神病性障碍患者人格的影响,为提高其长期疗效提供一些可行性措施。方法:通过前瞻性对照研究,将康复期精神分裂症、抑郁症患者随机分成研究组和对照组,研究组采用改良森田疗法联合药物治疗,对照组单用药物治疗,治疗1个月前后分别评定明尼苏达人格问卷(MMPI)、阳性和阴性症状量表(PANSS)、汉密尔顿抑郁量表(HAMD)。结果:研究组精神分裂症患者除D量表外,其他MMPI量表的T分均比治疗前显著降低,抑郁症患者除Mf、Ma量表外,其他量表T分也比治疗前显示降低(P均<0.05)。研究组治疗前后Hs、D、Hy、Pa、Pt、Sc、Si量表T分减分值与对照组比较,差异有统计学意义(P均<0.05)。结论:改良森田疗法有助于转变康复期精神病性障碍患者的某些异常人格特质。     

309名高中生MMPI测查结果分析

为研究高中学生这一群体的心理状态及存在的心理问题,应用明尼苏达多项个性测查表(MMPI)调查了309名高中生。结果发现男生Pt、Sc、Ma、Si量表原始分,女生Pt、Sc、Pa量表原始分明显高于中国常模原始分。随年龄增大及年级增高Pt、Sc、Pa、Ma量表分升高。Pt、Sc、Pa、Ma为超划界分量表,表明高中学生存在着相当多的心理状态偏离和明显的心理问题。     

明尼苏达多相个性测验结果在焦虑症患者个性特性的应用研究

目的探讨焦虑症患者的人格特征,为焦虑症的早期发现及治疗提供帮助同时为临床心理干预提供参考依据。方法采用MMPI(明尼苏达多相个性测验)量表对150例焦虑症患者(病例组)进行测试并与正常人群(对照组)进行比较。结果 4个效度量表中T分值均没有大于70分、Q、L在两组间得分分别小于30分、10分,所测结果有效。临床量表的比较中,病例组和对照组的Ma、Mf得分差异不具有统计学意义(P>0.05);病例组的Hs得分最高,病例组和对照组的Hs、D、Hy、Pd、Pa、Pt、Sc、Si比较两组间差异具有统计学意义(P<0.05)。结论焦虑症患者具有疑病、抑郁、偏执、精神衰弱等人格特点,MMPI在焦虑症患者早期发现,临床心理干预及治疗有一定指导意义。     

69例强迫症患者的MMPI分析

69例强迫症男、女患者的MMPI分析显示量表D、Hy、Pt、Sc、Pd、Pa、Hs、和F的原始分均分高于对照组差异显著,特别是前4个。其剖图以美国常模处理呈Sc-D-Pt-F量表高分和Ma最低分组合,中国常模呈量表D-Pt高分和Ma最低分组合。69例患者中、美常模剖图分析呈抑郁样反应的分别为66～64％,呈神经症样反应的为19～29％,呈分裂症样反应的为2～6％,正常剖图为11～2％。男、女患者的结果分析无显著差异。本症患者以中国常规处理较为适切。     

精神分裂症患者父母亲个性的研究

本文对60例精神分裂症患者的54位父亲,50位母亲和60位正常人的36位父亲,40位母亲进行TMMPI测验,结果发现:1.精神分裂症患者父母的Hy、Pd分量表分均高于正常对照组父母亲;患者父亲的Hs分量表与患者母亲的Pa分量表分分别高于正常对照组的父亲和母亲。2.精神分裂症患者与他们母亲的Pa、Sc分量表分呈正相关。3.精神分裂症妄想型患者的父母亲的Pa、Pt、Sc、Ma、Si分量表分比非妄想型患者的父母亲低。4.痊愈组患者父母亲比好转组患者父母亲的Hs、D、Hy、Pd、Pa、Pt、Sc分量代表分低。     

精神分裂症患者及其一级亲属性格特征的对照研究

目的探讨精神分裂症患者及其一级亲属的性格特征。方法选取住我院治疗处于缓解期的精神分裂症患者48例和一级亲属与正常组各79人，进行MMPI测查分析。结果精神分裂症患者及其一级亲属Hs、D、Hy、Pd、Pa、Pt、Sc量表分高于正常人，而患者和一级亲属间各量表分接近。结论精神分裂症患者及一级亲属具有明显的分裂性人格，两者的性格特征可能有着共同的遗传学基础。     

正常人和住院精神分裂症患者MMPI-2测图的对比分析

目的　分析住院精神分裂症患者MMPI 2测图的特点 ,考察划界分。方法　对正常人12 4 5例 (男 6 75例 ,女 5 70例 )和精神分裂症患者 6 12例 (其中男 36 1例 ,女 2 5 1例 )进行了MMPI 2测查结果进行分析。结果　男性除K、Ma量表外 ,女性除K量表外 ,正常组和精神分裂症组其他量表都存在显著差异 ;在划界分为样本 6 0T分时 ,男性、女性精神分裂症组双高点都为 6 8/86 ;划界分为样本 6 0T分、美国常模 6 5T分在鉴别正常组和精神分裂症组MMPI 2测图的效果基本接近 ,但两者双高点有明显不同 ,使用双高点鉴别精神分裂症将会有非常高的假阴性 ;划界分为样本 6 5T分时 ,鉴别精神分裂症组效果较差 ;用判别分析法有较好的鉴别效果。结论　分析中国人MMPI 2时 ,使用 6 0T分作为划界分比较合适 ;正常人与精神分裂症患者MMPI 2测图存在很大的差异。MMPI 2在临床上应该更适合作为一个人格量表使用 ,而不是作为诊断工具     

精神分裂症患者一级亲属MMPI心理状况调查

目的 调查了解精神分裂症患者一级亲属心理状况.方法 116名精神分裂症患者一级亲属接受明尼苏达多相个性测查表（MMPI）测查.结果 男性一级亲属MMPI量表中诈病（F）、校正（K）、社会内向（Si）因子低于常模水平,疑病（Hs）、抑郁（D）、癔症（Hy）、精神病态（Pd）、精神分裂（Sc）因子高于常模水平（P＜0.05）;女性一级亲属MMPI量表中诈病（F）、校正（K）因子低于常模水平,说谎（L）、疑病（Hs）、癔症（Hy）、精神病态（Pd）、精神衰弱（Pt）、轻躁狂（Ma）因子高于常模水平（P＜0.05）.结论 精神分裂症患者一级亲属心理健康程度较差.     

阻塞型睡眠呼吸暂停综合征患者情绪障碍的研究进展

在临床中睡眠呼吸暂停综合征患者患抑郁、焦虑的概率较高,而且同时患有抑郁、焦虑及OSAS的患者比仅患有OSAS患者病情更重。尽管许多研究评估了OSAS与情绪障碍间的关系,OSAS及情绪障碍之间一些可能的因果机制也已被提出,但是OSAS在情绪障碍的因果关系仍不清楚。对于OSAS伴焦虑抑郁状态的患者,情绪障碍的干预治疗有助于改善OSAS患者的嗜睡、疲劳症状及认知功能,提高患者生活质量。     

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.     

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.     

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。     

癫痫与自杀

自杀而导致死亡被为是增加癫痫患者死亡率的最重要原因之一。国外许多研究报道都表明癫痫患者的自杀率比普通人群的自杀率高几倍到二十几倍。可能导致癫痫患者自杀的危险性因素是有多方面的,本文将从5-HT、抗癫痫药及癫痫手术治疗、精神病理等方面对癫痫患者可能存在自杀危险因素进行综述,并希望在癫痫的综合治疗中对这些危险因素能加以考虑。     

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.     

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.     

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。