老年焦虑抑郁障碍共病54例临床研究

目的 探讨老年焦虑抑郁障碍的临床特征、诊断及治疗方法.方法 选取54例符合入组标准及排除标准的患者进行临床研究,归纳临床症状并进行统计分析.用汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)进行评分,对比治疗前后的评分变化,并以HAMA和HAMD减分率判定疗效.结果 老年焦虑障碍多与抑郁共病,躯体主诉多为其主要特点.治疗后第2周末开始起效,疗效随时间延长同步上升,治疗后第2、4、8周末HAMA、HAMD量表评分与治疗前比较,有显著性差异(P ＜0.05,P＜0.01).药物及心理治疗的总有效率90.75％.结论 老年焦虑障碍多与抑郁共病,及时干预治疗效果满意.     

重复经颅磁刺激对抑郁障碍患者睡眠质量改善的临床研究

研究背景 目前抑郁障碍患病率呈逐年升高之趋势,综合性医院就诊的抑郁障碍患者多以躯体化症状为主诉,尤以睡眠障碍最为常见,改善睡眠质量成为迫切的需要.本研究探讨重复经颅磁刺激(rTMS)对改善抑郁障碍患者睡眠质量的疗效.方法 以躯体化症状就诊的抑郁障碍患者随机分为单纯药物治疗组(药物治疗组)和rTMS联合药物治疗组(联合治疗组),分别采用汉密尔顿焦虑量表(HAMA)和抑郁量表(HAMD)评价两种治疗方法的疗效.结果 两种治疗方法在不同观察时间点,各项评分差异均有统计学意义(P=0.000),且治疗方法与观察时间点之间存在交互作用(均P=0.000).与药物治疗组相比,联合治疗组患者治疗1、2和4周时HAMA评分、HAMD总评分和躯体化症状评分降低(均P=0.000);治疗1周时睡眠障碍评分降低(P=0.001);治疗1和2周时抑郁症状评分降低(均P=0.000).与治疗前相比,药物治疗组患者各项评分除治疗后1周差异无统计学意义(P＞0.05)外,其余各观察时间点差异均有统计学意义(P=0.000);联合治疗组患者治疗后各项评分差异均有统计学意义(P=0.000).治疗后1、2和4周,两组治疗总有效率比较,联合治疗组[63.64％(14/22)、86.36％(19/22)、90.91％ (20/22)]高于药物治疗组[20％ (4/20)、55％ (11/20)、75％(15/20)],差异有统计学意义(均P=0.000).结论 重复经颅磁刺激联合药物治疗抑郁障碍患者起效早、效果好,尤其对睡眠质量的改善优于单纯药物治疗,可以提高抑郁障碍患者的治疗依从性.     

帕金森病患者情绪障碍研究

目的 了解帕金森病患者伴发的情绪障碍.方法 采用汉密尔顿焦虑评价量表和抑郁评价量表对100例帕金森病患者和50例对照者进行情绪障碍研究;并根据简易智能状态检查量表、帕金森病统一评价量表(UPDRS Ⅲ)和改良Hoehn-Yahr分级,分别评价帕金森病患者的认知功能和运动障碍严重程度并进行病情分级.结果 帕金森病组患者汉密尔顿焦虑评价量表评分[(14.45±8.30)分]和抑郁评价量表评分[(7.98±6.24)分]均高于对照组[(3.68±3.23)分、(2.76±3.32)分],差异均有统计学意义(P<0.01);其焦虑症状发生率为49%(49/100),高于对照组(2%),差异有统计学意义(P<0.01),但早期与中晚期患者之间差异无统计学意义(P>0.05).帕金森病组患者抑郁症状发生率(12%)虽高于对照组(2%),但组间差异无统计学意义(P>0.05);中晚期患者抑郁症状发生率高于早期者(P<0.05).帕金森病组焦虑症状主要表现为精神性焦虑及躯体性焦虑,抑郁症状则以焦虑躯体化、认知障碍、迟缓以及睡眠障碍为主;性别与肢体发病侧别对情绪障碍无明显影响,而汉密尔顿焦虑评价量表(r=0.199,P=0.049;r=0.295,P=0.005)和抑郁评价量表(r=0.196,P=0.050;r=0.274,P=0.009)情绪均与病程和UPDRSⅢ评分呈正相关.结论 帕金森病患者以焦虑情绪为主要情绪障碍症状,表现为躯体性焦虑和精神性焦虑,于疾病早期即已出现;而抑郁症状多出现于疾病的中晚期,主要表现为焦虑躯体化、认知障碍、迟缓以及睡眠障碍.     

治疗不敏感性抑郁症的临床特征与治疗转归

目的探讨治疗不敏感性抑郁症的临床特征与治疗转归。方法采用前瞻性的研究方法对入组的147例抑郁症患者进行随访,共124例患者完成整个研究。在治疗前、治疗1、2、4、6周末进行症状评估,评估工具包括汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、简明精神病量表(BPRS)、临床疗效总评量表、副反应量表。结果(1)A、B、C、D4组治疗有效率分别为86.21%、86.96%、50.00%和58.33%,但A组的脱落率较高,达18.69%;(2)治疗敏感性抑郁症患者的症状指标在随访3(7±1)d即有下降;而治疗不敏感性抑郁症患者在随访4(14±1)d才下降,治疗前精神性焦虑症状相对较轻,均分约少1.2分,治疗后遗留较多症状,具体为HAMD的焦虑/躯体化、阻滞、HAMA的精神性焦虑、躯体性焦虑、BPRS的焦虑忧郁、缺乏活力、激活性。结论不敏感性抑郁症患者治疗前精神性焦虑症状较轻,症状改善较慢,治疗后遗留较多抑郁焦虑的症状。     

抑郁与焦虑共病障碍临床研究

目的:调查抑郁与焦虑共病障碍的发生率,探讨其特点及预后.方法:对150例抑郁障碍患者用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、社会功能缺陷筛选量表(SDSS)和临床疗效总评量表(CGI)评定,3个月后进行随访.结果:45.3%的抑郁障碍患者共病焦虑障碍,共病以广泛焦虑障碍与惊恐障碍为最多(分别为22.0%、13.3%);入组时及3个月末,共病组HAMD、HAMA、CGI及SDSS总分均显著高于抑郁组(P＜0.05),3个月末共病组HAMA减分率显著低于抑郁组(P＜0.05),HAMD减分率两组差异无显著性.结论:抑郁与焦虑共病障碍发生率高,具有抑郁及焦虑症状重、社会功能损害重,焦虑症状不易缓解等特征.     

心理动力性心理治疗合并药物治疗对焦虑障碍患者防御方式的影响

目的 了解心理动力性心理治疗合并药物治疗对焦虑障碍患者防御方式的影响.方法 本研究26例符合DSM- IV诊断标准的焦虑障碍患者进行6个月的心理动力性心理治疗合并药物治疗,对患者进行治疗前后防御方式问卷(DSQ)、汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)评定及比较.结果 6个月重测时HAMD(4.79±5.86)和HAMA(5.42±7.204)均较治疗前(17.88±11.01)、(19.67±8.35)明显降低(t1=6.143,t2=6.989,P＜0.000).6个月后不成熟防御方式的评分下降显著(t=2.17,P=0.04);成熟型防御机制的评分增高显著(t=-4.84,P＜0.000);中间型防御机制评分下降显著(t=2.24,P=0.035).HAMA减分率与不成熟因子分下降率呈正相关(r=0.426,P=0.038).结论 心理动力性心理治疗合并药物治疗对焦虑障碍患者的焦虑和抑郁症状均有改善,并在改变症状的同时减少了不成熟防御机制的使用.心理动力性心理治疗合并药物治疗较单纯药物治疗更有助于焦虑症患者康复.     

丁螺环酮与文拉法辛在广泛性焦虑症患者中的血药浓度及疗效的比较

目的探讨丁螺环酮与文拉法辛在广泛性焦虑症患者中的血药浓度及疗效对比。方法研究选取2013年6月~2016年6月期间在我院接受治疗的100例广泛性焦虑症患者作为对象。随机将患者分为丁螺环酮组、文拉法辛组。比较两组患者汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表(HAMD)及焦虑自评量表(SAS)评分,血药浓度与治疗效果间的关系,有效率及不良反应。结果两组患者经药物治疗后HAMA、HAMD及SAS评分均有下降(P0.05);文拉法辛组患者HAMA、HAMD及SAS评分均低于丁螺环酮组(P0.05)。两组患者治疗后精神性焦虑及躯体性焦虑评分较治疗前明显降低(P0.05);文拉法辛组患者治疗后精神性和躯体性焦虑评分均明显低于丁螺环酮组(P0.05)。两组患者的临床疗效和血药浓度均无明显相关性,且不良反应发生率无明显差异(P0.05)。结论文拉法辛与丁螺环酮治疗广泛性焦虑症均有较好的治疗效果,不良反应较低,但是文拉法辛抗焦虑治疗的效果优于丁螺环酮。     

轻性抑郁障碍临床特征分析

目的了解轻性抑郁障碍的临床特征。方法采用自制一般情况调查表、抑郁自评量表(self-rating depression scale,SDS)、汉密尔顿抑郁量表(Hamilton depresssion scale,HAMD)24项版本、汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)及社会功能缺陷量表(social disability screening schedule,SDSS)分别对符合美国精神障碍诊断与统计手册第4版(DSM-Ⅳ)诊断标准的35例轻性抑郁障碍(研究组)和56例重性抑郁障碍(对照组)患者进行评定,比较两组的差异。结果研究组SDSS总分、抑郁自评量表(SDS)总粗分、汉密尔顿抑郁量表24项版本(HAMD24)总分及体重、认识障碍、日夜变化、阻滞、睡眠障碍、绝望感等因子分值低于对照组(P0.01),同时抑郁情绪、有罪感、自杀、早醒、工作和兴趣减退、阻滞、体重减轻、自知力障碍、日夜变化、人格或现实解体、偏执症状、绝望感等症状出现的频率也均低于对照组(P0.01),而躯体性焦虑、全身症状、疑病等症状出现的频率及HAMA躯体性焦虑因子分值均高于对照组(P0.05或P0.01);研究组有88.57%的患者首次就诊于非精神科,明显高于对照组(P0.01)。结论轻性抑郁障碍患者躯体症状相对较多,而抑郁情绪及社会功能缺陷程度相对较轻,首次多在非精神科就诊。     

团体认知行为治疗对抑郁症的临床疗效的评价

目的评价团体认知行为治疗合并抗抑郁药对社区轻度抑郁症的临床疗效。方法社区轻度抑郁症患者随机分为抗抑郁药物合并团体认知行为治疗(研究组42例)和抗抑郁药物治疗(对照组40例),于治疗前、治疗12周及24周评定汉密顿抑郁量表(HAMD-17)、汉密顿焦虑量表(HAMA)及临床疗效总评量表。结果 HAMD-17、HAMA及CGI总分及各因子时间主效应均存在统计学意义;HAMD-17总分及焦虑/躯体化分及睡眠障碍因子分、HAMA总分及各因子分及CGI评分组间主效应均存在统计学意义。结论抗抑郁药物治疗及抗抑郁药物合并团体心理治疗均能有效改善抑郁症状,合并组改善更明显。     

曲唑酮对酒依赖患者焦虑抑郁症的疗效观察

目的 探讨曲唑酮对酒依赖患者焦虑抑郁症状的有效性.方法 采用随机数字表法将70例符合酒依赖伴发抑郁障碍患者分为研究组和对照组各35例.对照组给予临床常规戒酒治疗,研究组合用曲唑酮治疗,疗程8周,分别于入组时、治疗后第2、4、6、8周末进行汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表(HAMD)、饮酒问卷(ADS)和密西根酒精依赖调查表(MAST)评定.结果 自第2周末起两组HAMA、HAMD评分比较差异均有统计学意义(P＜0.05).自第4周末起两组ADS、MAST评分比较差异均有统计学意义(P＜0.05).结论 曲唑酮能有效治疗酒依赖伴发的焦虑抑郁症状,降低饮酒欲望,强化酒依赖治疗效果.     

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.     

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.     

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。     

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.     

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.     

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,