运动神经元病临床神经电生理检查的研究进展

运动神经元病（motor neuron disease,MND）是以损害脊髓前角、脑干脑神经运动核和锥体束为主的一组慢性进行性变性疾病,包括了肌萎缩侧索硬化症（ALS）、进行性脊髓性肌萎缩症（PSMA）、脊髓性肌萎缩症（SMA）、进行性延髓麻痹（PBP）、原发性侧索硬化症（PLS）。发病率为2～3/10万,目前没有确实有效的治疗手段,从有症状开始,平均仅能存活3～5年。临床诊断主要依靠临床表现、神经电生理检查和神经影像学检查。     

消化道Cajal间质细胞介导肠神经传递的研究进展

消化道Cajal间质细胞(ICC)与胃肠运动功能关系密切。ICC根据形态和功能主要分成三种类型。ICC超微结构与肠神经联系紧密,形态学和功能学研究证实ICC介导肠神经的胃肠道作用。     

食管肠神经系统调控的研究进展

食管受到各级神经系统及体液的调控,而完成蠕动与收缩功能.食管的活动有赖于肠神经系统(enteric nervous system,ENS)的调控协调作用.食管存在着兴奋性神经元和抑制性神经元两种,他们通过多种神经递质相互作用而决定食管的紧张度、蠕动与收缩.对食管神经机制的理解及研发新型药物治疗食管功能紊乱和胃食管反流有重要意义.本文综述近十年来食管脑神经系统的研究进展.     

肠神经系统重塑的研究进展

研究证实,肠神经系统（ENS）是一个独立的整合系统,虽然也受中枢神经系统（CNS）调控,但可独立进行信息传递及程序处理,协调肠道的整体行为,因此被喻为“肠脑”。随着ENS研究的逐渐深入,发现ENS的重塑与某些疾病的病因、临床表现乃至治疗有着密切联系。本文将近年来相关重塑表现及影响因素的研究作一简要综述。     

肠神经系统退行性变的研究进展

肠神经系统(enteric nervous system,ENS)可独立调节胃肠道感觉、分泌和运动功能,ENS退行性变可导致胃肠道功能的异常,引起一系列的临床症状,其与胃肠动力性疾病和功能性胃肠病的发病有关。本文就导致ENS退行性变的原因、肠神经元退行性变引起的功能异常及其与临床症状的关联性、可能的治疗靶点等方面的研究进展作一概述。     

酚酞对大鼠结肠动力及肠神经系统的影响研究

目的 探讨长期应用酚酞对结肠肌电及肠神经系统(ENS)的影响。方法 建立大鼠“泻剂结肠”模型，应用电生理、组化及免疫组化技术研究酚酞对大鼠结肠动力、ENS多种神经递质及Cajal间质细胞(ICC)的影响。结果 大鼠饲以酚酞3个月后，结肠慢波频率减慢，结肠肌间丛还原型烟酰胺腺嘌呤二核苷磷酸黄递酶阳性神经细胞数目增多，乙酰胆碱酯酶阳性神经细胞数目减少，一氧化氮合酶免疫反应性增强，生长抑素免疫反应性减弱，肌间丛ICC分布不均匀，突起连接杂乱。结论 长期应用酚酞对结肠动力和ENS有损害作用，在临床治疗顽固性便秘时应避免长期应用酚酞等刺激性泻剂。     

神经干细胞移植治疗神经系统疾病的实验研究进展

自20世纪90年代以来,神经干细胞的研究,给生命科学带来了重大的变革.尤其对帕金森病、癫痫、痴呆等神经系统退行性病变以及脑缺血损伤后的修复治疗,具有较好的疗效.现将神经干细胞移植治疗神经系统疾病的实验研究状况简述如下.     

卒中后痉挛神经电生理改变的研究进展

脑卒中发生后会对脑组织发生不可逆的损伤,对肢体、言语、认知等功能造成不同程度的影响,由于脊髓前角α和γ运动神经元的高级中枢控制的丧失,对低级中枢的抑制和控制削弱,牵张反射亢进,肢体出现不同程度的痉挛,这会严重影响患者运动功能的恢复。评定是康复治疗的重要基础,精准有效地评估患者的痉挛状态对于指导其功能恢复、评价疗效及预测功能状态均有重要作用,然而痉挛的检查与评定方法在临床应用十分有限。本文通过文献回顾的方式,梳理了痉挛的产生机制并分析痉挛患者神经电生理改变的特点,总结了电生理指标变化与痉挛的关系,旨在为卒中后痉挛评估方法的选择提供参考,为卒中痉挛患者的康复治疗提供新思路。     

肠易激综合征发病机理的研究进展

肠易激综合征的发病机制至今仍不明确，目前比较一致的观点认为IBS是胃肠动力异常、内脏感觉敏感性增高、肠道感染、炎症、心理社会精神因素、神经免疫内分泌及基因遗传等多种发病机制共同参与共同作用的结果，本文就近年来有关IBS发病机制的研究进展作一综述。     

肠神经系统与重症急性胰腺炎胃肠动力紊乱机制的研究进展

重症急性胰腺炎(servere acute pancreatitis,SAP)是临床上常见的急重症之一,即使当今对疾病的诊疗技术已有高度的发展,SAP的病死率仍高达16.3%[1].大量的临床观察及动物实验发现,在SAP的早期病程中即可出现胃肠动力紊乱表现如麻痹性肠梗阻等.     

出血性休克对大鼠肠道运动功能及肠神经的影响

目的观察出血性休克(HS)对大鼠小肠推进率和离体小肠收缩活动的影响以及此病程中肠神经的变化。方法将52只雄性SD大鼠随机分为对照组(n=26)和HS组(n=26)。HS组在给予重度出血性休克后行复苏,对照组大鼠给予相同麻醉及插管,但不行休克。复苏6h后处死大鼠。两组大鼠处死前30min伊文斯蓝灌胃测定小肠推进率;检测离体空肠自发收缩活动及对河豚毒素(TTX)的收缩反应;观察两组肠肌间神经丛(MP)中PGP9.5免疫荧光染色的差异。结果 HS组小肠推进率明显低于对照组(P0.05)。与对照组相比,HS组离体空肠自发收缩的振幅显著降低(P0.05)。加入TTX后,对照组空肠自发收缩的曲线下面积显著降低(P0.05),而在HS组则无显著变化。与对照组相比,HS组MP中PGP9.5的阳性面积(P0.05)及累积光密度(P0.05)均显著降低。结论 HS可损伤大鼠小肠动力功能,MP中肠神经元的破坏可能是造成肠道运动功能障碍的神经源性机制。     

The enteric nervous system and neurogastroenterology

Neurogastroenterology is defined as neurology of the gastrointestinal tract, liver, gallbladder and pancreas and encompasses control of digestion through the enteric nervous system (ENS), the central nervous system (CNS) and integrative centers in sympathetic ganglia. This Review provides a broad overview of the field of neurogastroenterology, with a focus on the roles of the ENS in the control of the musculature of the gastrointestinal tract and transmucosal fluid movement. Digestion is controlled through the integration of multiple signals from the ENS and CNS; neural signals also pass between distinct gut regions to coordinate digestive activity. Moreover, neural and endocrine control of digestion is closely coordinated. Interestingly, the extent to which the ENS or CNS controls digestion differs considerably along the digestive tract. The importance of the ENS is emphasized by the life-threatening effects of certain ENS neuropathies, including Hirschsprung disease and Chagas disease. Other ENS disorders, such as esophageal achalasia and gastroparesis, cause varying degrees of dysfunction. The neurons in enteric reflex pathways use a wide range of chemical messengers that signal through an even wider range of receptors. These receptors provide many actual and potential targets for modifying digestive function.     

Understanding and controlling the enteric nervous system

The enteric nervous system or the 'Little Brain' of the gut controls gastrointestinal motility and secretion, and is involved in visceral sensation. In this chapter, new developments in understanding the function of the enteric nervous system are described. In particular, the interaction of this system with the interstitial cells of Cajal, the pacemaker cells of the gut, is highlighted. The importance of the interaction between the enteric nervous system and the immune system is discussed, especially in relation to functional bowel disorders and post-operative ileus. Evidence is also provided that neurones can change their function and phenotype, a phenomenon called neuronal plasticity, which contributes to the pathogenesis of visceral hypersensitivity. Finally, new developments in stem cell transplantation are described. All these new insights should lead to a better understanding of the enteric nervous system and hopefully to better ways of controlling it.     

Plasticity in the enteric nervous system

Enteric ganglia can maintain integrated functions, such as the peristaltic reflex, in the absence of input from the central nervous system, which has a modulatory role. Several clinical and experimental observations suggest that homeostatic control of gut function in a changing environment may be achieved through adaptive changes occurring in the enteric ganglia. A distinctive feature of enteric ganglia, which may be crucial during the development of adaptive responses, is the vicinity of the final effector cells, which are an important source of mediators regulating cell growth. The aim of this review is to focus on the possible mechanisms underlying neuronal plasticity in the enteric nervous system and to consider approaches to the study of plasticity in this model. These include investigations of neuronal connectivity during development, adaptive mechanisms that maintain function after suppression of a specific neural input, and the possible occurrence of activity-dependent modifications of synaptic efficacy, which are thought to be important in storage of information in the brain. One of the applied aspects of the study of plasticity in the enteric nervous system is that knowledge of the underlying mechanisms may eventually enable us to develop strategies to correct neuronal alterations described in several diseases.     

Inflammatory neuropathies of the enteric nervous system

Inflammatory neuropathy of the enteric nervous system is emerging as an important topic in the field of neurogastroenterology. Enteric ganglionitis can be either primary or secondary to a wide array of diseases (i.e., paraneoplastic, infectious, and neurological disorders) and is characterized by a dense infiltrate of inflammatory/immune cells mainly confined to the neural microenvironment. The clinical picture reflects the involved segment of the gastrointestinal tract (achalasia, gastroparesis, pseudo-obstruction, and megacolon). In these settings, symptoms may develop either acutely (frequently after a flulike episode in otherwise previously healthy individuals) or more slowly (e.g., in paraneoplastic syndromes). The inflammatory/immune response in enteric ganglionitis leads to neuronal dysfunction and degeneration over time and sometimes results in a complete loss of enteric neurons. The diagnosis of enteric ganglionitis is supported by detection of circulating antineuronal antibodies against select molecular targets, including Hu and Yo proteins, neurotransmitter receptors, and ion channels. Potential mechanisms involved in neuronal dysfunction include viral antigen expression in the enteric neural environment, molecular mimicry (onconeural antigens), and the role exerted by cellular and humoral autoimmunity. A short course of steroid or other immunosuppressive therapy has been shown to be helpful in the treatment of these conditions. This feature reinforces the concept of a cause/effect relationship of the immune-mediated insult damaging the enteric innervation. An increased awareness of the clinical features and the immunologic and neurodegenerative mechanisms of these forms of peripheral neuropathy is important to correctly diagnose this problem during the early stages of the disease process and to provide appropriate immunosuppressive therapies.