锥体外通路(一)

锥体外通路是指在随意运动通路(锥体系)以外的所有自动运动通路,包括从大脑皮质到各级运动神经元的一系列结构,并是由一系列短轴突的神经元所构成,参与肌张力、姿势及自动与随意运动的调整。锥体外系与锥体系虽为人体运动通路的两个不同组成部分,但却互为补充、影响,也正是在锥体外系的密切配合的基础上,才能保证人体得以完成各种有目的的、准确的随意运动。     

三七总皂甙通过细胞外信号调节蛋白激酶1/2信号通路促进大鼠

背景：三七总皂甙对骨髓基质细胞向神经样细胞分化的效应及相关信号通路目前尚不明确。 目的：探讨细胞外信号调节蛋白激酶1/2信号通路对三七总皂甙调节大鼠骨髓基质细胞向神经细胞增殖、分化的作用。 设计、时间及地点：细胞学体外观察,于2008-05/10在汕头大学医学院分子生物学实验室完成。 材料：4~6周龄雄性SD大鼠9只,由汕头大学医学院实验动物中心提供。三七总皂甙为广西梧州制药集团股份有限公司产品,细胞外信号调节蛋白激酶的抑制剂PD98059为Cell Signaling Tech 公司产品。 方法：全骨髓法体外分离纯化大鼠骨髓基质细胞,取传至第3代细胞进行诱导分化,设立3组：单纯诱导组向培养液中加入10 μg/L碱性成纤维细胞生长因子,预诱导24 h后全量换为正式诱导液(含10 μg/L碱性成纤维细胞生长因子、2% DMSO、200 μmol/L丁羟回醚的α-MEM培养基),每24 h半量换诱导液1次;三七总皂甙组向预诱导液和正式诱导液内加入终浓度100 mg/L三七总皂甙;PD98059组在三七总皂甙组培养液基础上加入10 μmol/L PD98059。 主要观察指标：细胞形态学观察,MTT法检测细胞增殖情况,免疫组织化学方法鉴定细胞Nestin的表达。 结果：诱导6 h后,少数细胞呈锥形,细胞突起增多伸长,类似神经元,继续诱导培养后细胞突起增多,突起相互连接成网状。与单纯诱导组、PD98059组比较,诱导6,12,24 h三七总皂甙组细胞均明显增殖(P < 0.05),且随诱导时间延长呈递增趋势(P < 0.05);单纯诱导组、PD98059组间比较无明显差异(P > 0.05)。与单纯诱导组比较,诱导24 h后三七总皂甙组Nestin阳性率明显升高(P < 0.05),PD98059组Nestin阳性率明显降低(P < 0.05)。 结论：三七总皂甙可以促进骨髓基质细胞的神经分化和分化后增殖,细胞外信号调节蛋白激酶1/2的特异性抑制剂PD98059能够拮抗三七总皂甙促增殖分化作用,提示细胞外信号调节蛋白激酶1/2信号通路是三七总皂甙促进骨髓基质细胞向神经细胞分化和增殖的重要环节。     

深部脑刺激电极埋置术治疗帕金森病(4例报告)

目的：探讨深部脑刺激电极埋置术治疗帕金森病的治疗效果。方法：使用微电极导向立体定向技术,在丘脑底核埋置深部电极,通过可控性电刺激治疗帕金森病的僵硬-震颤症状,结果：电刺激治疗帕金森病能有效控制患者的僵硬-震颤症状,能消除由药物引起的开-关现象和症状波动,服用的L-DOPA类药物可一定程度的减量,术中及术后无明显的并发症,结论：STN放置深部脑刺激电极,通过适当强度的电刺激,能使症状明显改善,并发症少,与损毁术相比相对安全,价格较昂贵。     

内嗅皮质-海马神经投射通路的形成——体内及体外示踪研究(英文)

目的:本研究对内嗅皮质- 海马通路的各个亚支的发生进行了调查。方法:对不同龄大鼠脑用DiI、DiO、快兰示踪法及calretinin 免疫细胞化学法处理。结果:槽通路、海马交通通路于胚胎16 天(E16)开始发生,而穿通通路分别始见于胚胎17天海马的腔隙分子层和生后第2天齿状回外分子层。DiI的逆行标记显示内嗅皮质-海马通路主要来自内嗅皮质中II到IV层神经元。另外,calretinin免疫细胞化学法显示Cajal-Retzius (CR)细胞早在胚胎16天存在于海马的腔隙分子层,DiI和calretinin免疫细胞化学法双重标记显示CR细胞和内嗅皮质转入纤维之间可能存在密切的接触关系。结论:嗅皮质-海马通路的各个亚支是按照上述各自的时间表进行发生,CR细胞和穿通纤维的发育时空关系提示该细胞对内嗅皮质传入纤维寻径具有引导作用。     

双侧丘脑底核脑深部电刺激术治疗帕金森病(附33例报道)

目的总结双侧脑深部电刺激术(DBS)治疗帕金森病(PD)的手术方法和效果。方法对具有严重双侧症状和轴性症状的33例PD病人进行同期双侧丘脑底核DBS治疗。采用磁共振扫描结合微电极记录技术进行靶点定位。术后采用统一帕金森病评定量表(UPDRS)运动评分评价刺激效果。结果术后随访3个月~4年,平均7.3个月。脉冲发生器开启时,UPDRS运动评分平均改善率在“关”状态下为62.3%,在“开”状态下为24.2%。记忆力下降2例,情绪改变7例,睁眼困难1例,肢体异动15例;无明显的致残性永久并发症和副作用。结论双侧丘脑底核DBS手术的安全性较高,可明显改善PD病人的运动功能。     

急性硬脊膜外脓肿(附4例报告)

脊髓硬膜外脓肿为椎管内硬脊膜外脂肪组织和静脉丛的化脓性感染,引起硬脊膜外间隙内大量脓汁积聚及肉芽组织增生,造成脊髓受压,出现相应的脊髓受压表现,属急性脊髓压迫症,此病不十分常见,易误诊。本文就有关问题并结合经手术证实的４例病人的体会报告如下。１　临床资料４例均为男性,年龄１５～３８岁,平均２９．２５岁。诱因：２例有皮下脓肿,１例有腰部封闭史,１例间歇发热３０天,腹痛１０天。前驱症状主要有发热、乏力及局部原发灶组织红、肿、热、痛。２例持续１０天左右,１例间歇发热３０天,另１例无明显前驱症状。首发症…     

外伤性双侧硬脑膜外血肿(附30例报告)

目的总结外伤性双侧硬脑膜外血肿(TBEDH)的临床特点和早期诊治办法。方法对30例TBEDH的临床特点、影像学检查结果、治疗方法和结果进行回顾性总结。结果30例中24例血肿位于中线旁,6例血肿位于中线两侧不同部位。14例伤后首次CT扫描明确诊断,16例表观为进展性,经手术或再次CT扫描确诊。30例均行手术清除血肿,27例为静脉性出血。出院时根据GOS评分恢复良好25例,中残3例,重残1例,死亡1例。结论TBEDH多见于前后方向着力者,多为静脉性出血；早期诊断和处理与预后密切相关。     

硬脊膜外囊肿二例报告

硬脊膜外囊肿二例报告赵贵德，魏明海，常鹏飞，侯菊生，孙树杰，宁丰，吴东升，白灿明我科最近连续遇到２例罕见的硬脊膜外囊肿，现报告如下。例１男，２５岁。四个月前无明显诱因腰腿痛，向两股内侧放射，腰部有束带感，三个月前双下肢无力，行走困难，但大小便正常，于...     

外泌体对脑缺血/再灌注损伤后星形胶质细胞炎症和MAPK-Cx43信号通路的影响

目的 探讨内皮细胞来源外泌体对脑缺血/再灌注(I/R)损伤后星形胶质细胞炎症和P38丝裂原活化蛋白激酶(P38 MAPK)-缝隙连接蛋白43(Cx43)信号通路的影响.方法 分离人脐静脉内皮细胞来源的外泌体(HUVEC-Exo).将SD大鼠分为假手术组、大脑中动脉闭塞(MCAO)组、HUVEC-Exo治疗MCAO(HU...     

Notch通路对缺氧诱导N9小胶质细胞释放炎症因子的调节作用

目的 应用γ-分泌酶抑制剂(DAPT)抑制Notch信号通路活化,探讨Notch信号通路在缺氧诱导小胶质细胞释放炎症因子中的作用. 方法 将体外培养的N9小胶质细胞分4组:常氧组、缺氧组、常氧+ DAPT组和缺氧+DAPT组.常氧+DAPT组与缺氧+DAPT加入10 μmol/LDAPT处理12h,常氧组和缺氧组加入等量溶剂,缺氧组、缺氧+10 μmol/L DAPT组同时进行缺氧处理12 h (3％O2).提取各组细胞mRNA及蛋白,实时定量PCR检测各组细胞白介素(IL)-6、IL-1β、肿瘤坏死因子-α(TNF-α) mRNA水平,Western blotting检测Notch信号通路中Notch1胞内段(N1ICD)、Hes1、Hey1蛋白水平,并运用ELISA法检测各组细胞IL-6、IL-1β、TNF-α分泌水平. 结果 DAPT对炎性因子IL-6、IL-1β、TNF-α mRNA及蛋白分泌具有抑制作用,并随着浓度的增加,抑制作用增大.分组处理12h后,缺氧组炎性因子IL-6、IL-1β、TNF-α mRNA及蛋白分泌水平较常氧组明显升高,Notch通路信号分子N1ICD、Hes1、Hey1水平升高,差异有统计学意义(P＜0.05);与缺氧组比较,缺氧+DAPT组炎性因子IL-6、IL-1β、TNF-α mRNA及蛋白分泌水平降低,Notch通路信号分子N1ICD、Hes1、Hey1水平降低,差异有统计学意义(P＜0.05);常氧+DAPT组与常氧组比较,上述指标差异均无统计学意义(P＞0.05). 结论 Notch信号通路参与调控缺氧诱导的小胶质细胞炎症介质的释放.     

Two cases of neuroleptic-induced prolonged extrapyramidal symptoms

Neuroleptic-induced extrapyramidal symptoms (EPS) are generally categorized as acute, withdrawal and tardive EPS. Here, we report two cases of a unique late-onset, long-lasting EPS (e.g., prolonged EPS); in those cases, EPS appeared a few months following initiation of haloperidol and lasted for a few months after significant reduction or complete withdrawal of neuroleptics. Case 1, a 41-year-old female, began to exhibit EPS such as bradykinesia, rigidity and parkinsonian gait 4 months after the haloperidol treatment. Her rigidity was ameliorated by a reduction of haloperidol; however, reduction of neuroleptics made it difficult for her to maintain a seated posture because of an imbalance of muscle tonus. Her EPS continued for 9 months even after haloperidol was switched to very low doses of thioridazine (10?mg/day). Case 2 is a 42-year-old female. She exhibited EPS including dysphagia and a difficulty in opening her mouth 3 months after the haloperidol treatment began. Her EPS lasted for 45 days, even after complete withdrawal of neuroleptics. The EPS observed in these two cases occurred even after prolactin levels became normal. “Prolonged EPS” is a unique subclass of neuroleptic-induced reversible EPS that might involve the coexistence of hypo- and hyper-dopaminergic transmission, especially in patients who show very low tolerance to neuroleptics.     

Two siblings with Allgrove's syndrome and extrapyramidal features

We report two siblings with Allgrove's syndrome and extrapyramidal features. Though various neurological abnormalities have been described in this disorder, we report the first patient of Allgrove's syndrome associated with dystonia and chorea.     

Dopamine transporter (DAT) genotype (VNTR) and phenotype in extrapyramidal symptoms induced by antipsychotics

INTRODUCTION: Impaired dopamine transporter (DAT) function may be involved in antipsychotic (AP)-induced extrapyramidal symptoms (EPS). A polymorphism involving a variable number of tandem repeats (VNTR) has been described in the DAT gene (SLC6A3). OBJECTIVE: We studied whether the SLC6A3 VNTR polymorphism is a risk or protection factor for AP-induced EPS. We also investigated the relationship between the polymorphism and DAT availability in the schizophrenic patient's brain. METHODS: Sixty-one patients receiving AP therapy participated in the EPS study. Of these, thirty-two cases presented EPS (Simpson-Angus >3) and twenty-nine without EPS (Simpson-Angus < or =3). The DAT expression was studied in fifteen AP-naive patients by [(123)I] FP-CIT SPECT. RESULTS: No significant differences were observed for the more common alleles ((*)9R and (*)10R) or for genotype frequencies between patients with EPS and those without EPS. The frequency of the (*)9R and (*)10R alleles was similar to that described in other European populations. There were no significant differences in striatal DAT binding among the three major VNTR genotype groups. CONCLUSIONS: Our results suggest that the VNTR polymorphism did not influence AP-induced EPS and did not affect DAT gene expression or protein function.     

The endocrinology of extrapyramidal system disorders

The study of endocrinologic changes in Parkinson's disease, Huntington's disease, and tardive dyskinesia may elucidate the pathophysiology of these disorders, especially the presence of hypothalamic lesions. There is probably a decrease in PRL concentrations in Parkinson's disease, and there may be an increase in TSH response to TRH stimulation. It is not clear if there is any change in GH concentrations in Parkinson's disease. There appears to be a robust increase in GH concentrations in Huntington's disease, and there may be a small increase in PRL as well. At present no endocrinologic abnormality has been well documented in tardive dyskinesia.     

The basal ganglia in extrapyramidal dysfunction

The rapid advances in knowledge of basal ganglia circuitry and function in recent years have allowed the construction of a functional scheme to explain many facets of known pathologic states. The dichotomy of Parkinson's disease; akinesia with increased tone, and the mirror effects in Huntington's disease; hemiballismus and tardive dyskinesia, hyperkinesia with decreased tone are explained as due to two outputs of the system with an intervening inhibitory neuron which reverses the sign. The two outputs control different motor functions; pallidothalamic involved primarily with movements and nigrobrainstem involved primarily with muscle tone.