帕金森病、运动神经元病同属神经系统变性疾病,临床表现明显不一,前者以运动迟缓、静止性震颤、肌强直、姿势障碍为主要特征,后者以损害上、下运动神经元部位不同组合表现,特征为肌无力和萎缩、延髓麻痹及锥体束征.两者极少复合存在,我院近来遇见1例帕金森病、运动神经元病复合存在,临床非常罕见,现报道如下: 1 病例简介 患者,男,76岁,小学文化.6年前患者出现行走困难,步行前倾,渐行走不稳,独自步行困难,并出现双上肢震颤,未行诊治;近1年患者步行不能,双上肢震颤加重,全身无力并四肢肌肉萎缩,卧床、生活不能自理,并伴反应迟钝、进食呛咳、吞咽困难,无胡言乱语,无头昏头痛,无恶心呕吐,无肢体抽搐,有便秘及小便潴留,于2015年1月22日入院.有高血压史,血压控制可,无家族遗传疾病及长期毒物接触史.查体:神清,口齿欠清,反应迟钝,能对答,颅神经阴性,双上肢肌力4级,双下肢肌力3级,四肢肌张力齿轮样增高,双上肢及右下肢有静止性震颤,四肢肌肉萎缩明显,以大小鱼际肌、肢带肌萎缩为甚,双侧感觉对称存在,双侧腱反射+,病理征阴性,双侧指鼻试验、跟膝胫试验不能完成.

吉兰-巴雷综合征(Guillain-Barre syndrome，GBS)是一类自身免疫介导的急性炎性周围神经病，年发病率为(1~2)/10万[1]，其临床表现复杂多变，但均以肢体对称性迟缓性瘫痪为主要表现，其次为感觉障碍、颅神经损害、自主神经功能损害等，常有脑脊液蛋白-细胞分离现象，而以感觉障碍为首发表现，且无蛋白-细胞分离的病例，国内尚未见报道，我院近来收治1例，报道如下。

>糖尿病神经病变是糖尿病的常见并发症,多为慢性远端对称性多神经病。以糖尿病酮症酸中毒(diabeticketoacidosis,DKA)为首发表现的糖尿病合并急性炎性脱髓鞘性多发性神经病(AIDP),或称为吉兰-巴雷综合征(GBS)。临床罕见,我院近来收治1例,现报道如下。临床资料患者女性,27岁,农民。2012年2月27日因"食欲不振、呕吐3 d,意识模糊1 d"收入我院内分泌科。近期无服用或接触毒物史,无疫苗接种史,无上呼吸道感染、发热、腹泻等。近1个月体重明显下降。入院体检:血压78/55 mm Hg(1 mm Hg=0.133 kPa),嗜睡,心肺正常,腹软,

目的 探讨促红细胞生成素(EPO)对血管性痴呆(VaD)大鼠海马CA1区胆碱乙酰转移酶(ChAT)的影响.方法 将经行为学筛选合格的Wistar大鼠随机分为假手术组(Sham组)、VaD组、EPO侧脑室注射+VaD组(E1组)和EPO腹部皮下注射+VaD组(E2组),采用永久性结扎双侧颈总动脉的方法建立VaD模型.通过免疫组织化学和RT-PCR方法检测VaD大鼠海马CA1区ChAT蛋白含量以及ChAT mRNA表达水平的变化.结果 EPO能明显改善VaD大鼠认知功能障碍,上调海马CA1区ChAT表达.结论 EPO可能通过增加VaD大鼠海马区ChAT表达改善其认知功能障碍.

神经血管单元将脑微血管系统与神经元紧密联系起来,呈现调节脑血流量及控制血脑屏障物质交换等多重功能,是维持脑微环境稳定的重要结构.证据表明,神经血管单元的病变与阿尔茨海默病的发病过程密切相关；以神经血管单元作为靶向为阿尔茨海默病的治疗研究显现了新的思路.

目的:探讨促红细胞生成素(EPO)对血管性痴呆(VaD)模型大鼠海马神经细胞凋亡的影响.方法:将经行为学筛选合格的Wistar大鼠分为假手术组、VaD组、EPO组,采用永久性结扎双侧颈总动脉的方法建立VaD模型.应用TUNEL染色检测大鼠海马的凋亡细胞数;通过免疫组化学和RT-PCR方法,检测大鼠海马Bcl-2和Bax蛋白以及其mRNA表达水平的变化.结果:EPO能明显抑制海马神经细胞凋亡,上调Bcl-2表达,抑制Bax表达.结论:EPO可能通过调控VaD大鼠海马Bcl-2和Bax表达,从而抑制神经细胞凋亡.

Cognitive dysfunction has been a critical disease which affects the health and quality of life(QOL) of the elderly.Early intervention can delay the cognitive failure and the development of behavior problems in patients, and it can maintain fundamental cognitive function and improve the QOL of patients as well as caregivers.This review describes the progress of Alzheimer's disease and other cognitive dysfunction.

1986年Reimer等发现,间断的短暂缺血对后续的长时间缺血非但不产生累积损伤效应,反而起一定的保护效应.Murray等经研究证实了这一结果,并首次提出了"缺血预处理"的概念.嗣后,人们对缺血预处理的机制进行了广泛研究,并证实缺血预处理后机体释放内源性信号物质,通过一些中介物的介导从而产生保护作用.现从信号转导的角度对脑缺血预处理保护作用的分子机制综述如下.

The clinical manifestations of drug-induced neuromuscular diseases are different with the types of drugs and the pathogenesis of which involved the direct toxic effects of drugs, dysimmunity, protein synthesis blocked and impaired mitochondrial function. Since drug-induced neuromuscular diseases can be cured, early diagnosis and treatment can directly affect the prognosis. It is necessary to raise the clinical awareness of drug-induced neuromuscular disease.

Many drugs can induce cognitive impairment. The affect of drug-induced cognitive impairment may be related to the dosage and the period of drug treatment. The recognization of the relationship between drugs and cognitive impairment is helpful to rational administration of drugs.

目的探讨精神分裂症与2型糖尿病间是否存在遗传相关性。方法纳入首发精神分裂症患者133例、正常一级亲属79名、2型糖尿病患者125例和正常对照88名,采用限制性片段长度多态性技术（PCR-RFLP）检测胞浆型磷脂酶A2（cPLA2）基因BanI多态性与断裂基因1（DISC1）rs821616多态性。比较上述4组间BanI与rs821616基因多态分布频率的差异。结果①精神分裂症组和2型糖尿病组BanI多态性的A2/A2基因型频率与正常对照组间的差异均有统计学意义（P=0.047,OR=2.419;P=0.043,OR=2.472）,A2/A2基因型频率分别为:精神分裂症组（17.29%）、一级亲属（13.93%）、2型糖尿病（17.60%）、对照组（7.96%）;A1/A2、A1/A1基因型和A1、A2等位基因频率组间比较差异均无统计学意义（P＞0.05）;②4组间rs821616多态性的基因型和等位基因分布频率差异均无统计学意义（P＞0.05）。结论cPLA2基因BanI多态性与精神分裂症和2型糖尿病均可能存在关联,提示cPLA2基因可能与两种疾病均相关;未发现rs821616多态性与精神分裂症或2型糖尿病关联。

Objective To explore the effect of intravenous injection of xeno-isotype bone marrow mesenchymal stem cells(BMSCs) on the cholinergic system of the hippocampus formation in Vascular Dementia(VaD) rats.Methods MSCs isolated and expanded in vitro were labelled with BrdU.Rats received permament bilateral carotid arteries ligation to establish VaD models and randomly divided into three groups.Group A: Rats were intravenously injected 3×106 MSCs at the fourth week after ligation;Group B: Rats were intravenously injected vehicle(PBS) at the same time;Group C: Sham group.BrdU labelled MSCs were observed by immuno-fluorescence and the activity of AChE and ChAT were tested at the fourth week after injection.Results BrdU-labelled MSCs were found in the hippocampus at the fourth week after intravenous injection.The activity of AChE and ChAT significantly increased in the hippocampus of rats in group A compared with group B(P0.05),although that in both of the groups significantly decreased compared with group C(P0.05).Conclusions MSCs improved the activity of cholinergic system in the hippocampus of VaD rats.

PURPOSE:To determine the influence of tanshinone on the levels of nitric oxide synthase (NOS) and acetylcholinesterase (AChE) in the brain of an Alzheimer's Disease (AD) rat model and on its potential therapeutic mechanism.METHODS:100 Male Sprague Dawley rats were divided into three groups: control group, model group and tanshinone treatment group. 10 microg A beta 1-42 was injected bilaterally into the dorsal lateral region of the dentate gyrus in the hippocampus of rats in the model and tanshinone treatment groups to prepare the AD models. 24h after modeling, tanshinone, 50mg/kg, was administered by gastric perfusion to rats in the tanshinone treatment group. Later, immunohistochemical assay and Western blot analysis were used to detect expression of neuronal NOS (nNOS) and inducible NOS (iNOS) in the rat hippocampus. Activity of AChE in each subregion (CA1 approximately CA4) of rats' hippocampus was determined by a histochemical technique.RESULTS:Expression of nNOS in the model group was down-regulated whereas iNOS was up-regulated. After A beta 1-42 injection, the number of AChE positive fibers in each subregion (CA1 approximately CA4) of the hippocampus was decreased compared with controls. With tanshinone administration, the changes were improved to varying degrees.CONCLUSION:Tanshinone modulates AChE and NOS proteins concentrations in the hippocampus of AD rats. This may have therapeutic potential in AD rats.

人们对血管病变影响认知功能的认识已逾一个世纪,并随研究的不断深化而先后萌生出动脉硬化性痴呆、多发梗死性痴呆和血管性痴呆(VaD)的概念.20世纪90年代血管性认知损害(VCI)概念的问世,为进一步研究创建了崭新的平台,但也衍生出不少新问题有待解决.

近十余年来,随着内源性大麻素的发现,探讨大麻素系统与神经系统疾病的关系已成为当前的研究热点,大麻素制剂用于神经系统疾病治疗的临床价值已初露端倪。随着研究的不断深入,大麻素系统有望成为神经系统疾病药物治疗的重要靶点。

维生素B12缺乏在临床上颇为常见,其发生率随年龄增长而增加[1].据统计在发达国家社区老年人维生素B12缺乏的患病率为120‰[1-5],而住院老人患病率则高达300‰～400‰[6]

目的探讨糖尿病对慢性脑低灌注大鼠的学习记忆能力和神经元损伤的影响。方法以链脲佐菌素诱导产生实验性糖尿病大鼠,双侧颈总动脉结扎建立慢性脑低灌注模型,应用Y-迷宫评价错误次数和全天总反应时间,HE染色观察各组大鼠海马CAl区神经元的数目,免疫组化法检测海马区CDK5表达,结合蛋白质印迹(Westernblot)实验对海马区CDK5蛋白作半定量分析。结果与单纯糖尿病和慢性脑低灌注组大鼠比较,糖尿病合并慢性脑低灌注组大鼠从2w开始,迷宫作业错误反应次数增多,全天总反应时间延长,海马CAl区神经元数明显减少,CDK5蛋白表达减少。结论糖尿病加重慢性脑低灌注导致大鼠学习、记忆能力下降和神经元损伤,可能与CDK5表达减少有关。

Objective: To investigate clinical significance of DSA on etiology diagnosis of stroke in young and middle-aged patients. Methods: Examination results of DSA of 160 young and middle-aged patients with stroke were analyzed retrospectively. Results: The pathogenesis of 126 patients was found through DSA examination, primary etiology was cerebral aneurism, cabined middle cerebral artery stenosis, AVM and Moya-Moya. Conclusion: DSA examination has important significance in young and middle-aged adults suffered stroke.

Objective To study the clinical features of multiple sclerosis(MS).Methods The general clinical data,leision locations,results of important assistant examinations,treatment of 168 MS patients were synthetically analyzed.Results The most common symptoms were weakness and dysesthesia.Secondly,they were muscle spasm and pain,vision dysfunction,incontinence,and ataxia.The rare symptoms were peripheral neurological changes.Laboratory examinations:Protein and IgG-index levels in CSF were markedly high.MRI abnormal ratio were 90.98%.The administration of glucocorticoid was effective.Conclusion There are a variety of clinical symptoms in patients with MS which mainly affect the white matter of central neurological system and showed multiple focus and multiple-phase course.In addition to clinical features,neuroelectrophysiology,CSF immunology and imaging investigations altogether care can greatly increase the rate of clinical definite diagnosis.Among them,MRI is relatively more useful.

Aim: To observe the changes in neuronal survival ability, protein expression and activity of cyclin-dependent kinase 5 (cdk5) in hippocampus cultured primarily exposed to hypoxia environment. Methods: The experiment was carried out in the Experimental Animal Center of Second Military University of Chinese PLA from January to December 2005. Neurons from the hippocampus of 14-18 day rat fetuses were cultured for 8-10 days, and then exposed to hypoxia environment for culture for 12, 24 and 36 hours, respectively. The survival ability of neurons was measured in a darkroom with micropore reader at 590 nm; cdk5 protein level was estimated with Western blot methods and the activity of cdk5 was estimated for three times. Results: Compared with the normal group, the survival ability of hippocampus neurons exposed to hypoxia environment was decreased significantly from 12 hours [(1.01±0.14), (0.77±0.15); (0.98±0.12), (0.68±0.11); (0.95±0.11), (0.61±0.08); P < 0.01], and the expression of cdk5 protein level in the hypoxia group was decreased significantly [(1.67± 0.19), (0.82±0.08), (1.54±0.13), (0.75±0.06); (1.49±0.13), (0.70±0.11); P < 0.01], while the activity of cdk5 was increased remarkably [(1.76, 3.56); (1.84, 4.29); (1.95, 6.04); P < 0.01]. Conclusion: Hypoxia could cause hippocampus injury, which may be related with the increased level of cdk5 activity.