非典型抗精神病药物所致恶性综合征的临床特征

本文目的是探讨非典型抗精神病药物所致恶性综合征(NMS)的临床特征,为临床早期诊断和治疗提供参考。抗精神病药物所致NMS是一种严重的药物不良反应,几乎所有的抗精神病药物均可引起。与典型抗精神病药物相比,非典型抗精神病药物所致NMS发生率更低、病情更轻、死亡率更低。不同种类非典型抗精神病药物所致NMS临床特点各异。对于老年人及应用抗抑郁药物者发生的NMS尤应引起重视,因为这些因素可增加死亡的风险。     

氯氮平引起恶性症状群

恶性症状群(NMS)一般由经典的抗精神病药物引起。氯氮平属非经典的抗精神病药物,也会引起NMS。本文报道一例因氯氮平引起的NMS。病人为30岁,因重性精神病用氯氮平治疗。在氯氮平治疗前一个月,已停用除氯羟安定以外的所有抗精神病药物,氯氮平从每天25mg,每日三次的剂量开始,第三次服药后3小时,病人出现了典型的NMS,突然高烧,多汗、严重的上肢齿轮样     

精神药物致恶性综合征32例临床分析

目的:了解精神药物所致恶性综合征(NMS)的临床特征,并探讨NMS发生的影响因素. 方法:对32例精神药物所致NMS患者进行临床分析. 结果:精神药物致NMS男性多见于女性,青壮年居多,传统抗精神病药、多种抗精神病药联用、增加剂量过快是产生NMS危险因素. 结论:临床应尽量减少合并用药、加量过速,以免导致NMS.     

第二代抗精神病药所致恶性综合征——读者来信

编辑先生: 恶性综合征(NMS)是抗精神病药可引起的一种凶险的不良反应,已有大量报道关于第一代抗精神病所引起的.有无利培酮等第二代抗精神病药引起的报道,请介绍,谢谢.     

氯氮平所致神经阻滞剂恶性综合征

氯氮平属二苯氧氮平类药物,是一种有相当疗效抗精神病药物,尤其是对其它抗精神病药物疗效不理想的某些精神分裂症患者,甚至会出现戏剧性效果。它具有较强的镇静作用,但几乎没有锥体外系副反应。一般认为它不会引起神经阻滞剂恶性综合症(NMS),因而对于既往有过NMS史的患者成为可选药物之一。然而近几年来,国内外有关氯氮平所致NMS已有多     

恶性综合征时的脑脊液单胺代谢

恶性综合征(NMS)是一种抗精神病药物治疗时潜在的致死性并发症。由于该病是由具有高效抗多巴胺作用的神经阻滞剂引起,近来人们的注意力已集中到中枢多巴胺活动减退与 NMS 发病机理二者之间的关系上,即 NMS 可能是由于纹状体和下丘脑的多巴胺活动降低所致,为了充分证实这一理论,作者测定了8例 NMS 患者 CSF 中多巴胺代谢物高香草酸(HVA)和5-羟吲哚乙酸(5-HIAA)、去甲肾上腺素(NA)和3-甲氧-4     

精神药物致恶性综合征32例I临床分析

目的：了解精神药物所致恶性综合征（NMS）的临床特征，并探讨NMS发生的影响因素。方法：对32例精神药物所致NMS患者进行临床分析。结果：精神药物致NMS男性多见于女性，青壮年居多，传统抗精神病药、多种抗精神病药联用、增加剂量过快是产生NMS危险因素。结论：临床应尽量减少合并用药、加量过速，以免导致NMS。     

静脉滴注氯丙咪嗪致恶性症候群5例[日]

恶性症候群(NMS)是抗精神病药物所致的严重副作用，早已被人们现熟知与阻断DA受体有关，用DA受体激动剂治疗有效。但最近报导认为不但是DA受体阻断强的抗精神病药物即使对DA受体阻断弱的或几乎没有阻断DA受体作用的抗抑郁药也能发生NMS，     

恶性综合征继发横纹肌溶解1例报道

正恶性综合征(neuroleptic malignant syndrome,NMS)是抗精神病药物所致的严重不良反应,主要表现为高热、肌强直、意识障碍及肌酶升高,好发于突然停用或更换抗精神病药物时[1-3]。我科2018年5月收治1例继发横纹肌溶解的NMS患者,本文分析其临床资料并进行文献复习,探讨NMS严重并发症的处理方法,以提高对该病的认识。     

抗精神病药物所致恶性症状群12例的临床资料分析

我们将抗精神病药物所致恶性症状群(NMS)12例的临床资料报道于后。     

心境稳定剂联合新型抗精神病药物在双相障碍中的应用

众多研究显示双相障碍的治疗趋向采用心境稳定剂（锂盐和丙戊酸钠）联合新型抗精神病药物（利培酮、奥氯平、喹硫平、齐拉西酮）治疗．可增加疗效且不良反应无明显增加。本文就心境稳定剂联合新型抗精神病药物治疗双相障碍的疗效及不良反应作一综述。     

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.     

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.     

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,     

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。     

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.