中学生有害使用苯二氮(艹,卓)类药物调查

目的:探讨中学生有害使用苯二氮革类药物的心理社会因素.方法:对109例有害使用苯二氮革类药物中学生进行自编调查表及艾森克个性问卷(EPQ)测定. 结果:有害使用苯二氮(艹,卓)类药物者在为普通学校,占71.56%.EPQ测定有害使用苯二氮革类药物者P分和N分偏高,主要原因有精神压力和同学影响.结论:中学生有害使用苯二氮革类药物与社会、家庭、学校多方面因素有关,应引起社会的重视并加以正确引导.     

卡马西平治疗甲唑安定的撤药症状

甲唑安定是一种短作用的三唑苯二氮(艹卓)类药物,目前认为是较理想的抗焦虑药,但是本药容易产生耐药性和药物依赖,而且撤药十分棘手。部份病人需要小剂量、缓慢地减药。就本文作者所知,还没有文章报告卡马西平对苯二氮类撤药症状及甲唑安定的撤药症状治疗有效。     

卡马西平治疗苯二氮(艹卓)类戒断症状

苯二氮(艹卓)类药物治疗期间可能出现的毒性作用与其治疗效果同样引起人们的极大关注。最近Klain等报导了3例不能耐受阿普唑仑逐渐减量的惊恐障碍患者,用卡马西平使其撤药。本文报导用卡马西平处理苯二氮(艹卓)类药物的戒断症状。     

门诊医源性苯二氮类药物依赖患者65例分析

目的调查我院门诊医患治疗关系在苯二氮类药物依赖患者形成中的作用。方法对符合苯二氮类药物依赖的65例病人进行自制项目及非苯二氮类药物替代治疗调查。结果超安全期使用苯二氮类药物治疗原发病,患者可较容易从多家医院或不同医生处获得苯二氮类药物;随时间推移患者对治疗药物依赖的兴趣及对药物不良反应的恐惧均下降;门诊医生对患者的用药及治疗情况难以实质性控制等,促进了医源性苯二氮类药物依赖的产生。结论门诊较为随意的医患治疗关系有利于医源性苯二氮类药物依赖的形成,却不利于其治疗。控制使用苯二氮类药物对原发性疾病治疗的时间是避免导致医源性苯二氮类药物依赖形成的简单而有效的方法。     

曲唑酮治疗苯二氮革类药物依赖和戒断反应的临床对照研究

目的探讨曲唑酮对苯二氮革类药物依赖性失眠的疗效和安全性。方法共40例苯二氮革类药物依赖性失眠患者,分为苯二氮革类联合曲唑酮组（曲唑酮组）和苯二氮革类联合安慰剂组（对照组）,逐渐减半苯二氮革类药物剂量,治疗3个月后根据HoItzman—Gellert戒断症状评分法、汉密尔顿焦虑量表（HAMA）和多导睡眠图监测结果评价曲唑酮戒断疗效,副反应量表（TESS）评价药物不良反应。结果与对照组比较,曲唑酮组患者自治疗后7d戒断症状评分开始降低（P=0．000）,自治疗后15dHAMA评分开始降低（P=0．000）;与治疗前比较,经曲唑酮治疗后两项评分均降低（P=0．000）。与对照组比较,曲唑酮组患者治疗后7d总睡眠时间和慢波睡眠时间延长、睡眠效率提高、睡眠潜伏期缩短（均P=0．000）;与治疗前相比,经曲唑酮治疗后总睡眠时间和慢波睡眠时间延长、睡眠效率提高、睡眠潜伏期缩短（均P=0．000）。未见明显不良反应,两组患者治疗前后TESS评分差异无统计学意义（P〉0．05）。结论曲唑酮治疗苯二氮革类药物依赖和戒断反应疗效显著,且安全性良好。     

中学生有害使用苯二氮类药物调查

目的 :探讨中学生有害使用苯二氮 艹卓 类药物的心理社会因素。　方法 :对 10 9例有害使用苯二氮 艹卓 类药物中学生进行自编调查表及艾森克个性问卷 (EPQ)测定。　结果 :有害使用苯二氮 艹卓 类药物者在为普通学校 ,占 71.5 6 %。EPQ测定有害使用苯二氮艹卓 类药物者P分和N分偏高 ,主要原因有精神压力和同学影响。　结论 :中学生有害使用苯二氮艹卓 类药物与社会、家庭、学校多方面因素有关 ,应引起社会的重视并加以正确引导     

门诊医源性苯二氮(艹卓)类药物依赖患者65例分析

目的调查我院门诊医患治疗关系在苯二氮(艹卓)类药物依赖患者形成中的作用.方法对符合苯二氮(艹卓)类药物依赖的65例病人进行自制项目及非苯二氮(艹卓)类药物替代治疗调查.结果超安全期使用苯二氮(艹卓)类药物治疗原发病,患者可较容易从多家医院或不同医生处获得苯二氮(艹卓)类药物;随时间推移患者对治疗药物依赖的兴趣及对药物不良反应的恐惧均下降;门诊医生对患者的用药及治疗情况难以实质性控制等,促进了医源性苯二氮(艹卓)类药物依赖的产生.结论门诊较为随意的医患治疗关系有利于医源性苯二氮(艹卓)类药物依赖的形成,却不利于其治疗.控制使用苯二氮(艹卓)类药物对原发性疾病治疗的时间是避免导致医源性苯二氮(艹卓)类药物依赖形成的简单而有效的方法.     

门诊医源性苯二氮(艹卓)类药物依赖患者65例分析

目的调查我院门诊医患治疗关系在苯二氮(艹卓)类药物依赖患者形成中的作用.方法对符合苯二氮(艹卓)类药物依赖的65例病人进行自制项目及非苯二氮(艹卓)类药物替代治疗调查.结果超安全期使用苯二氮(艹卓)类药物治疗原发病,患者可较容易从多家医院或不同医生处获得苯二氮(艹卓)类药物;随时间推移患者对治疗药物依赖的兴趣及对药物不良反应的恐惧均下降;门诊医生对患者的用药及治疗情况难以实质性控制等,促进了医源性苯二氮(艹卓)类药物依赖的产生.结论门诊较为随意的医患治疗关系有利于医源性苯二氮(艹卓)类药物依赖的形成,却不利于其治疗.控制使用苯二氮(艹卓)类药物对原发性疾病治疗的时间是避免导致医源性苯二氮(艹卓)类药物依赖形成的简单而有效的方法.     

苯二氮类药物长期使用的安全性

苯二氮艹卓类药物长期使用的安全性成都市精神卫生中心（６１００３６）周明康詹希贤秦小荣七十年代末期苯二氮艹卓类药物的使用量达到了空前的高峰，但从八十年代以来则急剧下降。长期使用苯二氮艹卓类药物的安全性如何？无疑是人们关注的焦点。当初苯二氮艹卓类药物取代...     

苯二氮卓类药物使用的注意事项

苯二氮卓类药物使用的注意事项读者来信编辑同志：苯二氮类药物在精神科临床上应用十分广泛，对不少病人有较好的疗效，请问在使用时有什么注意事项？扬州市一医师答读者来信扬州市一医师：在使用苯二氮类药物（ＢＺＤｓ）时应注意下列八个方面：一、适应症和禁忌症ＢＺＤ...     

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.     

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.