丙戊酸镁缓释剂合并帕罗西汀治疗难治性抑郁症对照研究

目的：观察丙戊酸镁合并帕罗西汀治疗难治性抑郁症组的疗效及安全性。方法：将50例难治性抑郁症患者随机分为合用组（丙戊酸镁缓释剂合并帕罗西汀）25例和单用组（帕罗西汀组）25例。疗程6周。分别评定汉密尔顿抑郁量表（HAMD）和治疗中出现的症状量表（TESS）。结果：合用组HAMD量表分于治疗3周显著下降,单用组HAMD分于治疗4周显著下降,合用组有效率显著高于单用组35％（P〈0．05）。结论：丙戊酸镁缓释剂合并帕罗西汀治疗难治性抑郁疗效确切。     

丙戊酸镁对广泛性焦虑的辅助治疗作用

目的：观察帕罗西汀联合丙戊酸镁治疗广泛性焦虑的疗效。方法：将60例广泛性焦虑患者随机分为两组,分别接受帕罗西汀联合丙戊酸镁（合用组）和帕罗西汀（单用组）治疗。疗程4周。分别于治疗前和治疗第1、2、4周末以汉密尔顿焦虑量表（HAMA）、临床疗效总评量表（CGI）评定疗效,治疗中出现的症状量表（TESS）评定药物不良反应。结果：治疗4周末,合用组HAMA评分显著低于单用组;合用组显效率显著高于单用组;两组不良反应均轻,发生率相仿。结论：帕罗西汀联合丙戊酸镁治疗广泛性焦虑有良好的疗效。     

抑郁症的增效治疗（二）——齐拉西酮对伴有精神病性症状抑郁症的治疗作用

目的：探讨齐拉西酮治疗伴有精神病性症状抑郁症的临床疗效。方法：60例伴有精神病性症状的抑郁症患者随机分为合用组28例（齐拉西酮联合帕罗西汀治疗）和单用组32例（单用帕罗西汀治疗）,疗程6周。采用汉密尔顿抑郁量表（HAMD）、简明精神病评定量表（BPRS）、临床疗效总评量表（CGI）和治疗中出现的症状量表（TESS）评定临床疗效和不良反应。结果：治疗后两组HAMD、BPRS及CGI评分均较治疗前明显下降（P〈0.05或P〈0.01）;两组比较,以合用组降低更为显著（P〈0.05或P〈0.01）。合用组TESS评分（2.11±1.20）分和单用组TESS评分（1.9±0.16）分差异无统计学意义（P〉0.05）。结论：齐拉西酮联合帕罗西汀治疗伴有精神病性症状的抑郁症临床疗效优于单用帕罗西汀。     

奥氮平对难治性抑郁症的辅助治疗作用

目的：观察奥氮平联合文拉法辛治疗难治性抑郁症的疗效和不良反应。方法：将92例难治性抑郁症患者随机分成两组，合用组为奥氮平联合文拉法辛，单用组为单用文拉法辛，疗程6周。以汉密尔顿抑郁量表（HAMD）和汉密尔顿焦虑量表（HAMA）评定临床疗效；以治疗中出现的症状量表（TESS）评定不良反应。结果：治疗后两组HAMD和HAMA的评分均显著降低（P〈0．01），以合用组疗效显著（P〈0．01或P〈0．05）。结论：奥氮平联合文拉法辛治疗难治性抑郁症的疗效优于单用文拉法辛，耐受性好。     

电针合并小剂量米氮平治疗老年抑郁症的疗效观察

目的观察电针合并小剂量米氮平治疗老年抑郁症的临床疗效和不良反应。方法随机将60例老年抑郁症患者分为电针合并米氮平治疗（合用组）和单用米氮平治疗（单用组）,各30例,治疗6周。采用汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）和治疗中出现的症状量表（TESS）评定疗效及不良反应。结果两组治疗后HAMD、HAMA评分均较治疗前有显著性差异（P〈0．01）;合用组在第1、2周末HAMD及HAMA减分率显著大于单用组,在第4、6周末两组减分率无明显差异;两组的显效率分别为80％和73．3％;主要不良反应合用组比单用组少而轻。结论两组治疗老年抑郁症均有较好疗效,前者起效快,不良反应少,依从性高。     

奎硫平合并丙戊酸镁缓释片治疗精神分裂症兴奋激越研究

目的：比较奎硫平合并丙戊酸镁缓释片与氟哌啶醇治疗精神分裂症患者伴有兴奋、激越症状的疗效及不良反应.方法：对精神分裂症住院患者采用随机对照、开放性研究治疗2周.以阳性与阴性症状量表（PANSS）及临床疗效总评量表（CGI）评估疗效,以治疗中出现的症状量表（TESS）评估不良反应.结果：合用组与对照组的总体疗效相当,兴奋、激越症状的控制前者优于后者（P＜0.05）;不良反应方面,氟哌啶醇引起的锥体外系不良反应较奎硫平合并丙戊酸镁缓释片高.结论：奎硫平合并丙戊酸镁缓释片对精神分裂症兴奋、激越症状的疗效优于氟哌啶醇,且不良反应较小.     

度洛西汀、米氮平、帕罗西汀与阿米替林治疗伴躯体症状抑郁症的对照研究

目的探讨度洛西汀、米氮平、帕罗西汀与阿米替林治疗伴躯体症状抑郁症的疗效和安全性。方法将符合国际疾病分类第10版（ICD一10）诊断标准的伴躯体症状的抑郁症患者117例,随机分为4组,分别给予度洛西汀、米氮平、帕罗西汀与阿米替林治疗,疗程8周。采用汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）和副反应量表（TESS）评定疗效及不良反应。结果4组药物均能迅速起效,第2周末HAMD、HAMA评分较治疗前差异有统计学意义（P〈0．05）,治疗8周后,4组闯疗效无统计学意义（P〉0．05）,4组HAMD、HAMA评分较治疗前有统计学意义（P〈0．01）,4个治疗组不良反应有统计学意义（P．〈0．01）。结论治疗伴躯体症状的抑郁症,四药总体疗效相似,均起效较快,度洛西汀、米氮平和帕罗西汀不良反应相对少,依从性好。提示四种药物均为治疗伴躯体症状的抑郁症一线药物,度洛西汀、米氮平和帕罗西汀值得临床推广。     

度洛西汀与舍曲林治疗伴有慢性疼痛抑郁症患者的疗效比较

目的观察度洛西汀与舍曲林治疗伴有慢性疼痛抑郁症患者的疗效。方法将60例伴有躯体疼痛症状的抑郁症患者随机分为度洛西汀组（30例）和舍曲林组（30例）,观察8周。采用汉密尔顿抑郁量表17项（HAMD）、研究用疼痛量表（MOSPM）和治疗时出现的症状量表（TESS）于治疗前及治疗后第1、2、4、8周末进行评定。结果度洛西汀组与舍曲林组改善抑郁症状总体疗效及不良反应无显著性差异（P〉0.05）,但治疗疼痛症状度洛西汀组总体疗效显著优于舍曲林组（P〈0.05）。结论度洛西汀治疗慢性疼痛的抑郁症患者安全有效,不良反应少,依从性好,度洛西汀起效时间较舍曲林快。     

丙戊酸镁缓释片治疗精神分裂症的辅助作用

目的:探讨阿立哌唑合用丙戊酸镁缓释片治疗难治性精神分裂症患者的疗效及安全性。方法:60例难治性精神分裂症患者随机分为两组,分别给予阿立哌唑合用丙戊酸镁缓释片与阿立哌唑单用治疗,疗程8周。用阳性与阴性症状量表(PANSS)和治疗中出现的症状量表(TESS)评定疗效和不良反应。结果:阿立哌唑合用丙戊酸镁缓释片治疗难治性精神分裂症的疗效优于单用阿立哌唑(P<0.05);两组不良反应差异无统计学意义(P>0.05)。结论:阿立哌唑合用丙戊酸镁缓释片治疗难治性精神分裂症疗效好,安全性好。     

西酞普兰与奎硫平治疗伴躯体症状抑郁症观察

目的:探讨西酞普兰联合奎硫平治疗伴有躯体不适主诉的抑郁症患者的疗效与安全性。方法:收集伴有躯体不适主诉的抑郁症患者68例,随机分成合用组(西酞普兰加用奎硫平)和单用组(单用西酞普兰),以汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、临床疗效总评量表(CGI)、副反应量表(TESS)在治疗1、2、4、6周时各评定1次。结果:治疗6周末,两组HAMD和HAMA评分均显著低于治疗前。治疗第4、6周末两组间HAMD、HAMA评分差异有极显著性(P<0.01及0.05)。合用组有效率86%,显著优于单用组的有效率62%。结论:西酞普兰联合奎硫平治疗伴躯体症状的抑郁症疗效好,安全性高。     

度洛西汀与马普替林治疗抑郁症临床对照研究

目的探讨度洛西汀在治疗抑郁症中的疗效及副反应。方法采用随机分组的方法，将符合CCMD--3诊断标准的120例抑郁症患者分为度洛西汀组和马普替林组各60例。两组患者均用药治疗观察8周。采用汉密尔顿抑郁量表（HAMD）、临床疗效总评量表（CGI—SI）及副反应量表（TESS）评定。结果通过8周的开放性对照研究后发现，度洛西汀与马普替林疗效相当（P〉0．05），且副反应少；、结论度洛西汀是治疗抑郁障碍的理想药物。安全有效、可作为首选药物，具有不良反应少、依从性好的特点。     

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.     

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.     

头痛 呕吐伴意识不清简

病历摘要 患者男性,48岁。主因突发头痛、呕吐伴意识不清18h,于2013年4月21日入院。入院前18h无明显诱因突发头痛,呈全脑爆发性剧痛,伴非喷射状呕吐,呕吐物为胃内容物和暗红色血性液体。发病后意识状态呈渐进性下降,至入院前2h处于昏迷状态,呼之不应,刺激四肢无反应。病程中无双眼凝视、口角歪斜、肢体抽搐等症状。     

Tissue with high intelligence quotient Adipose-derived stem cells in neural regeneration

The aim of the present review is to highlight the possible neuroregenerative potential ol adipose-derived stem cells. The key property of stem cells is plasticity including self-renewal, multilineage differentiation, and migration, whereas the required property is transplantability. For a long time, embryonic stem cells were thought to be the only source of pluripotency, a dogma that has been challenged during the last decade. Today, an alternative option might be adipose-derived stem cells, as easily accessible, ethical and autologous cellular source. Recent knowledge of adipobiology increasingly recognizes that adipose tissue is the major endo- and paracrine organ of the human body. Likewise, numerous neuropetides, neurotrophic factors, neurotransmitters, hypothalamic and steroid hormones and their receptors are shared by adipose tissue and brain. Accordingly, the regenerative potential of neuroprotective factor-secreting adipose-derived stem cells is outlined. Whether the possible benefits of adipose stem cell-based therapy may be mediated via cell transdifferentiation and/or paracrine mechanisms remains to further be evaluated.     

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.     

31例中枢神经系统真菌感染临床分析

目的 分析中枢神经系统真菌感染患者的临床特征、预后及其影响因素.方法 对31例中枢神经系统真菌感染患者的诊断与误诊、实验室和病原学检查、治疗与预后等进行回顾性统计分析.结果 31例患者中合并其他疾病者21例,占67.7%.首诊误诊23例,占74.2%.19例患者脑脊液墨汁染色发现隐球菌,占61.3%;17例隐球菌培养阳性,占54.8%.两性霉素B（AmpB）治疗者16例,其中5例在疾病早期联合氟康唑治疗,4例联合氟胞嘧啶（5-Fc）,单用氟康唑13例.治愈16例,占51.6%;好转7例,占22.6%;死亡8例,占25.8%.结论 中枢神经系统真菌感染误诊率高;各种原因所致的免疫缺陷是引发中枢神经系统真菌感染的主要危险因素;尽早明确诊断、联合AmpB与5-Fc抗真菌治疗、积极控制颅内压是降低病死率、改善预后的关键.     

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.