恶性肿瘤患者围手术期情绪分析

目的：探讨恶性肿瘤患者围手术期情绪障碍动态变化特征。方法：用抑郁自评量表(SDS)、焦虑自评量表(SAS),观察55例恶性肿瘤患者住院不同时段情绪障碍的检出率及临床特征。结果：70％左右患者存在抑郁情绪。不同时段的焦虑、抑郁症状不同。结论：恶性肿瘤患者围手术期情绪障碍明显,需要予以干预。     

冠状动脉内支架植入术治疗患者的情绪障碍及心理干预

目的　了解冠状动脉内支架植入术 (PTCA)治疗前后患者的情绪障碍和心理干预的效果。方法　在手术前后对患者进行心理干预 ,并用汉密顿焦虑量表 (HAMA)和汉密顿抑郁量表 (HAMD)在心理干预前后对患者进行测查。结果　心理干预前患者有明显的焦虑抑郁情绪 ,心理干预后患者的焦虑抑郁情绪明显改善。结论　心理干预是减轻PTCA治疗患者焦虑抑郁情绪障碍的有效方法 ,值得广泛应用     

多发性硬化患者抑郁焦虑障碍与生活质量的关系

目的　探讨多发性硬化 ( multiple sclerosis,MS)患者中抑郁焦虑情感障碍发生率及抑郁焦虑与患者生活质量评定的关系。方法　采用汉密尔顿抑郁量表 ( HAMD)、汉密尔顿焦虑量表 ( HAMA)及 Spitzer生活质量指数 ( Spitzer quality of life index,QLI)量表 ,对 5 8例 MS患者及 5 0名健康人进行调查评分 ,并记录扩展的残疾状况评分 ( EDSS)和病程时间。应用多重回归统计方法对上述各项进行相关分析。结果　 MS患者抑郁情绪发生率为 48.3 % ( 2 8/5 8) ,焦虑情绪发生率为 3 2 .7% ( 1 9/5 8) ,抑郁合并焦虑发生率为 2 9.3 % ( 1 7/5 8) ,均较对照组明显升高 ( P <0 .0 1 ) ;生活质量较对照组明显减低 ( P <0 .0 1 )。抑郁焦虑情绪与生活质量有显著相关性 ,其中抑郁情绪为生活质量减低的重要预示因素。结论　MS患者中抑郁焦虑情感障碍发生率较高 ,抑郁焦虑情绪对生活质量评价有显著影响。     

80例脑梗死患者情绪障碍的调查分析

目的了解脑梗死患者的焦虑、抑郁情绪。方法用焦虑自评量表(SAS)和抑郁自评量表(SDS)对80例脑梗死患者进行调查,并与70名健康自愿者进行配比对照分析。结果脑梗死患者的焦虑抑郁总分明显高于对照组,患者中已确诊焦虑占48%,抑郁占49%。结论部分脑梗死患者有明显的情绪障碍,临床医师在治疗躯体疾病的同时还要注意患者的焦虑和抑郁症状。     

共患不宁腿综合征对偏头痛患者情绪和睡眠的影响

目的探讨偏头痛患者的不宁腿综合征(RLS)的发病率及其对情绪和睡眠的影响。方法对200例偏头痛患者(偏头痛组)和100名正常成人(对照组)进行RLS发病率、严重程度、睡眠质量和焦虑及抑郁程度评分,比较偏头痛人群与对照组之间的差异。并对共患有RLS的偏头痛患者的情绪和睡眠情况进行分析。结果成人慢性偏头痛组的RLS发病率(16.25%)较对照组(5%)高,差异有统计学意义(P0.05);发作性偏头痛组的RLS发病率(12.5%)与对照组(5%)比较,差异无统计学意义(P0.05)。共患RLS的偏头痛患者较单纯偏头痛者的睡眠质量差、焦虑及抑郁评分高,差异有统计学意义(均P0.05)。头痛频率及RLS为抑郁、焦虑及睡眠障碍的影响因素(均P0.05)。偏头痛患者的汉密尔顿抑郁量表(HAMD)评分、汉密尔顿焦虑量表(HAMA)评分及匹茨堡睡眠质量量表(PSQI)评分与国际RLS评估量表(IRLS)的相关系数分别为rHAMD=0.397、rHAMA=0.434和rPSQI=0.500;RLS严重程度与抑郁、焦虑及睡眠障碍的严重程度呈正相关关系(均P0.05)。结论慢性偏头痛患者的RLS发病率更高,且RLS症状更严重。RLS的严重程度与抑郁、焦虑和睡眠障碍程度呈正相关关系。     

酒依赖患者的情绪障碍和述情障碍

目的：探讨酒依赖患者的情绪障碍和述情障碍。方法：采用汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）、多伦多述情障碍量表（TAS）以50例酒依赖患者和50例正常对照组进行比较研究。结果：酒依赖组与对照组在焦虑、抑郁情绪和述情障碍方面存在明显差异。结论：纠正情绪和述情障碍可能有利于戒酒成功。     

神经反馈在卒中后抑郁和焦虑中应用的研究进展

卒中后情绪障碍发生率很高,严重的抑郁、焦虑对于患者的治疗、康复有着不同程度的消 极影响。神经反馈技术是通过对脑电参数的适应性训练,从而改善患者的情绪症状。目前应用神经 反馈干预卒中后抑郁、焦虑的研究相对较少,且对于干预脑区及脑波尚无统一定论。本文将对神经 反馈在卒中后抑郁、焦虑方面的应用加以综述。     

阻塞性睡眠呼吸暂停合并抑郁患者血清白介素-18变化的研究

阻塞性睡眠呼吸暂停综合征(obstructive sleep apneahypopnea syndrome,OSAS)是临床常见的睡眠障碍疾病,可引发多系统并发症及精神障碍,而抑郁是最常见的精神障碍,既往研究显示,OSAS及抑郁患者体内均存在炎症反应,而白介素-18(IL-18)作为一种重要的前炎性因子,在OSAS及抑郁患者体内均有不同程度的升高[1-2].我们通过测定OSAS及抑郁患者血清中IL-18的水平,探讨IL-18在OSAS合并抑郁的发生机制中所起的作用.     

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.     

重庆市儿童青少年焦虑抑郁发生情况调查

目的 调查重庆市儿童青少年焦虑抑郁发生情况,为儿童青少年学生心理疏导提供参考.方法 通过整群抽样选取儿童青少年学生425名,年龄范围为7～16岁,采用儿童焦虑性情绪障碍筛查量表及儿童抑郁障碍自评量表对被试进行评估.结果 ①34.6％(147/425)的青少年存在焦虑情绪,9.9％(42/425)的青少年存在抑郁情绪;5.6％(24/425)同时存在焦虑抑郁情绪,33.2％(141/425)仅有焦虑或抑郁情绪,61.2％(260/425)无情绪问题.②男性、女性间焦虑抑郁情绪分布差异具有统计学意义(x 2=12.592,P＜0.05),男性中66.1％的无任何情绪问题,25.3％仅存在焦虑情绪,5.6％仅存在抑郁情绪,3.0％存在焦虑抑郁情绪;女性中55.2％的无任何情绪问题,33.3％仅存在焦虑情绪,2.6％仅存在抑郁情绪,8.9％存在焦虑抑郁情绪.不同性别间焦虑得分差异具有统计学意义(t=4.638,P＜0.05),抑郁情绪得分差异无统计学意义(t=0.672,P＞0.05).③年龄与焦虑(r=-0.42,P＞0.05)、抑郁情绪(r=0.071,P＞0.05)间相关关系无统计学意义,焦虑情绪与抑郁情绪评分之间存在相关关系(r=0.420,P＜0.001).结论 儿童青少年焦虑抑郁发生率较高,需要给予积极心理关注.     

神经症、心境障碍、精神分裂症患者MMPI测查结果分析

目的探讨神经症、心境障碍、精神分裂症的MMPI调查问卷模式,并剖析三组患者心理特征,以协助临床医师进行诊断和治疗。方法采用病例对照研究,三组304例患者MMPI测试结果进行分析,同时选取100名健康被试进行对照研究。结果神经症与心境障碍患者,各量表分之间无显著差异;心境障碍组和精神分裂症组的各量表T分之间,L／F／Hs／Hy／Mf／Pa／Ma无显著差异,K／D／Pd／Pt／Sc／Si存在显著差异;精神分裂症组在Pt、Sc、Ma和Si,T分有所偏低。结论MMPI在神经症、心境障碍、精神分裂症之间有特异的临床特征和测图模式．     

阻塞性睡眠呼吸暂停低通气综合征及脑卒中与认知功能障碍的关系

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）是脑卒中的危险因素,脑卒中患者合并阻塞性睡眠呼吸暂停在流行病学上也远远高于普通人群的发病率.OSAHS及脑卒中都可以发生认知功能障碍,两者并存有可能加剧患者认知功能障碍程度及影响恢复,研究和了解OSAHS对卒中后认知功能的影响,对卒中相关认知障碍的防治有着重要的意义.     

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.     

农业治疗对精神分裂症患者主观睡眠质量的影响

目的探讨农业治疗对精神分裂症患者主观睡眠质量的影响。方法随机抽取广州市民政局精神病院男女各2个病区的住院精神分裂症患者作为研究对象,予以测评匹兹堡睡眠质量指数量表（PSQI）,评分〉7分判断合并有主观睡眠障碍,将此类患者随机分为两组,在原治疗药物不变的基础上,研究组加用农业治疗,对照组临睡前加用舒乐安定1～2mg,观察3个月,先后于入组前、治疗第1,2,3个月以PSQI及治疗中出现的症状量表（TESS）进行评定,判断治疗效果及药物不良反应。结果（1）300例患者中有74例PSQI评分〉7分,精神分裂症患者中主观睡眠障碍的检出率为24．7％;（2）研究的3个时间点两纽的PSQI评分均要低于入组前,差异有统计学意义（F=3．883,P=0．046）,但两组间的PSQI评分差异无统计学意义（F=0．504,P=0．552）;（3）研究组在治疗不良反应的严重程度及所引起的痛苦评分两方面要低于对照组（P〈0．05）。结论相对于舒乐安定,农业治疗更有利于精神分裂症患者的主观睡眠问题的改善,可尝试将农业治疗应用于有主观睡眠问题的精神分裂症患者。     

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.     

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。     

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.     

Effects of p75 neurotrophin receptor knockout on axonal regeneration in a mouse model of facial nerve injury

BACKGROUND： Previous studies have shown that p75 neurotrophin receptor plays an important role in peripheral nerve injury. However, the role of p75 neurotrophin receptor in the regeneration of peripheral nerves remains poorly understood. OBJECTIVE： To study the effect of p75 neurotrophin receptor on facial nerve regeneration. DESIGN, TIME AND SETTING： A randomized controlled experiment was performed in the Regeneration Laboratory of Flinders University, Australia and the Biomedical Laboratory of Dentistry School, Shandong University from March 2005 to February 2006. MATERIALS： Cholera toxin B subunit, fast blue, and biotin rabbit-anti goat IgG were provided by Sigma, USA; goat-anti choleratoxin B subunit ant/body was provided by List Biologicals, USA. METHODS： In p75 neurotrophin receptor knockout and wild type 129/sv mice, the facial nerves on one side were crushed. At days 2 and 4 following injury, regenerating motor neurons in the facial nuclei were labeled by fast blue, and the regenerating axon was labeled by the anterograde tracer choleratoxin B subunit. MAIN OUTCOME MEASURES： Axonal regenerative velocity and number were detected by immunohistochemical staining of choleratoxin B subunit, growth-associated protein, protein gene product 9.5, and calcitonin-gene-related peptide; survival of motor neurons in the facial nuclei was detected by retrograde fast blue. RESULTS： Axonal growth in the facial nerve of p75 neurotrophin receptor knockout mice was significantly less than in wild type mice. At day 7 after injury, the number of regenerating motor neurons in p75 neurotrophin receptor knockout mice remained significantly less than in wild type mice （P 〈 0.05）. The number of positively stained fibers for growth-associated protein-43, protein gene product 9.5, and calcitonin-gene-related peptide in p75 neurotrophin receptor knockout mice was significantly less than in wild type mice （P 〈 0.01）. CONCLUSION： p75 neurotrophin receptor promoted axonal regeneration and enhanced the survival rate of motor neurons following facial nerve injury.