显微外科技术修复周围神经损伤临床观察

目的 评价显微外科技术修复周围神经损伤的临床效果.方法 89例周围神经损伤患者均采用显微外科技术进行修复治疗,主要包括神经外膜缝合术、束膜缝合术及外膜束组膜缝合术,术后随访12～24个月,观察临床效果.结果 手术共修复113条神经,其中功能恢复优66条,良23条,可14条,差10条.外膜缝合组、外膜束组膜缝合组、束膜缝合组患者功能恢复优良率分别为81.4％、76.3％、78.1％,不同缝合方式间的功能恢复优良率差异无统计学意义(P＞0.05).结论 显微外科技术修复周围神经损伤能够促进患者神经功能的恢复,改善功能,应在临床进一步推广使用.     

显微镜下修复周围神经损伤疗效分析

我院自2004—2009年来应用显微外科技术修复周围神经损伤79例,共92条。术后经3～36个月随访,疗效满意。现汇报如下。1资料与方法1.1一般资料79例患者,男62例,女17例,年龄15～     

膝关节周围骨折合并神经损伤的处理

膝关节周围骨折是较为常见的关节内骨折,主要是外力撞击引起,常引起骨折分离移位,部分合并神经损伤,治疗不当易造成关节疼痛、畸形、僵硬、不稳或功能障碍等不良后果.作者自2003至今共收治15例膝关节周围骨折合并神经损伤患者,经采取合理有效的治疗方法,取得满意效果.     

产科围术期周围神经损伤120例治疗与分析

周围神经损伤为临床常见并发症,其会导致患者出现支配区功能障碍,影响正常生活,严重甚至引发患者出现残疾［1］。产科医师在临床治疗过程中,常会忽略围术期引发的周围神经损伤,导致出现医疗纠纷。本文通过对2011‐03—2014‐05在我院产科收治的120例患者随机分组,讨论产科围术期周围神经损伤的原因及治疗方法,现报告如下。     

周围神经损伤后修复的有关影响因素

周围神经损伤后修复的有关影响因素冯凯林世和赵节绪薛志刚周围神经损伤后，由于显微外科技术的应用，使得目前已能够十分精确地将中断的神经对合，但功能完全恢复者十分罕见。近几十年来，人们已从改进神经修复的纤维外科技术转向了探索神经再生过程中的细胞、分子和基因...     

周围神经损伤后不同时间的修复比较

背景：大量实验证明,Bungner带-许旺细胞-基底膜结构是神经再生理想的微环境。这一结构在神经损伤两三周后形成。而在神经损伤数小时后,近断端的神经纤维就开始发芽再生神经纤维开始再生与所需微环境的形成并不同步。 目的：观察周围神经损伤后不同时间进行修复的最佳效果。 设计、时间及地点：随机对照动物实验,于2007-06/2008-06在哈尔滨医科大学动物实验中心完成。 材料：新西兰大白兔20只,随机数字表法分为4组：2周后神经修复组、4周后神经修复组、3个月后神经修复组、即时神经修复组。 方法：建立成年新西兰大白兔周围神经损伤模型,即时修复组立即缝合伤口,2周后神经修复组、4周后神经修复组、3个月后神经修复组采用神经两断端分别固定于肌膜上,逐层缝合伤口,2周,4周,3个月后重新打开伤口,在手术显微镜下用10-0无损伤尼龙针线进行外膜缝合修复坐骨神经,缝合伤口。 主要观察指标：各组缝合神经段的神经电生理、轴突数、光镜及电镜观察结果。 结果：2周后神经修复组神经传导速度慢于4周后神经修复组、3个月后神经修复组(P < 0.01);即时神经修复组与2周后神经修复组差异无显著性意义(P > 0.05)。2周后神经修复组效果最好,神经纤维走行正常、排列完好,神经纤维可见血管增生,髓鞘结构较好,许旺细胞功能活跃,新生轴突内微丝密集排列。4周后神经修复组最差,神经纤维数量少、排列紊乱,髓鞘轴突变性明显,大部分神经纤维脱髓鞘崩解,轴突消失,未见再生神经纤维。3个月后神经修复组效果较差,可见较多神经纤维结构破坏,排列略紊乱,髓鞘和轴突变性较明显,仅见少量再生神经纤维,许旺细胞略少,胞质不发达。即时进行神经修复组效果较好,神经纤维结构破坏不明显,排列整齐,髓鞘和轴突变性轻,神经纤维内见有大量再生髓鞘,许旺细胞明显增多,胞质较发达。2周后神经修复组轴突计数优于其他3组(P < 0.05),4周后神经修复组最少。 结论：神经损伤2周后进行神经修复效果优于其他时间点,是周围神经损伤后修复的最佳时机。     

甲状腺素凝胶促进周围神经损伤修复的实验研究

目的 探讨甲状腺素凝胶对大鼠坐骨神经损伤修复的作用.方法 54只雄性SD大鼠双侧坐骨神经切断造成0.8 cm缺损,用甲壳素导管桥接神经缺损后随机分为3组,每组18只.A组管内注入甲状腺素凝胶,B组管内注入赋形剂明胶,C组管内注入等渗盐水.术后第4、8周分别检测各组运动神经传导速度(MNCV)并收集标本,行特殊染色、S -100免疫组织化学染色,观察再生神经的组织学变化,并进行统计学分析.结果 术后4、8周 A组神经传导速度优于B、C组,其差异有统计学意义(P＜0.05),B、C2组差异无统计学意义(P＞0.05);A组S -100免疫组织化学染色示阳性神经纤维数及特殊染色显示再生有髓神经纤维数均多于B、C组(P＜0.05),B、C组差异无统计学意义(P＞0.05).结论 局部应用甲状腺素凝胶可以促进周围神经的再生和功能恢复.     

腰椎骨折压迫神经损伤的临床观察

目的探讨胸腰椎骨折合并脊髓神经损伤的手术治疗时机及效果。方法随机抽取2014-03—2015-03本院收治的106例胸腰椎骨折合并脊髓神经损伤患者,所有患者均经临床检查确诊,并知情同意。将106例患者按照入院时间分为实验组(伤后72h内入院,n=52)与对照组(伤后72h后入院,n=54)。2组均实施手术治疗。术后随访12个月,对比治疗效果。结果实验组手术时间、术中出血量均多于对照组,差异有统计学意义(P0.05);术后随访12个月,实验组优良率100.0%(52/52),明显高于对照组的81.5%(44/54),差异有统计学意义(P0.05);2组患者术后椎管容积、Cobb角、伤椎前缘高度均优于术前,差异有统计学意义(P0.05),但组间对比差异无统计学意义(P0.05)。结论胸腰椎骨折合并脊髓神经损伤患者实施早期手术治疗,能获得较为显著的术后恢复效果。但早期手术所需手术时间较长,且术中出血量多。因此,在临床治疗过程中,需严格按照患者具体情况选择不同手术时机,以提升临床效果。     

神经电生理对周围神经损伤的评估价值探讨

目的探讨神经电生理对周围神经损伤的诊断价值。方法对160例有周围神经临床症状的患者行针极肌电图(EMG)、运动神经传导速度(MCV)和感觉神经传导速度(SCV)的检测,并与本实验室正常值对比。结果未见神经损伤者16例,轻度神经损伤者47例,中重度神经损伤者66例。完全性神经损伤者31例。结论神经电生理是周围神经损伤部位、程度、范围和预后的客观检查方法。     

损伤神经周围注射自体PRP对周围神经损伤的修复效果观察

目的 探讨损伤神经周围注射自体富血小板血浆(platelet-rich plasma,PRP)对周围神经损伤的修复效果。方法 选取2017年1月-2018年7月于本院接受治疗的周围神经损伤患者130例,随机分为手术组、PRP联合组各65例,手术组患者进行显微外科手术,PRP联合组患者在手术基础上注射自体PRP进行治疗; 用酶联免疫吸附实验法检测血清C反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)水平,用Western blot法检测胰岛素样生长因子1(IGF-1)、血管内皮生长因子(VEGF)表达水平,并对2组患者神经传导速度、下肢运动功能、基本功能优良率以及肌电图疗效进行检测。结果 治疗1、3、6、12个月后PRP联合组患者CRP、TNF-α水平均低于手术组,IGF-1、VEGF表达水平均高于手术组(P<0.05); 治疗1、3、6、12个月后PRP联合组患者感觉、运动神经传导速度、下肢运动功能评分、基本功能恢复优良率、肌电图愈显率均高于手术组(P<0.05)。结论 在手术治疗的基础上注射自体PRP对周围神经损伤患者进行治疗,能够减轻患者炎性损伤程度,上调IGF-1、VEGF的表达水平,加快神经传导速度,促进患者下肢运动功能恢复     

修复周围神经损伤的神经移植材料

摘要：周围神经大段损伤一直是康复领域的重大难题,所以修复损伤的周围神经逐渐成为热点话题。在众多的修复方法中,移植修复周围神经损伤已经成为研究热点。自体移植物是临床上的“黄金标准”,人工组织工程材料移植物来源广泛,同种异体移植物可避免异体移植造成的免疫排斥反应。文章采用文献收集及总结的方法,探讨了自体移植物,人工组织工程材料移植物和同种异体移植物的研究进展。 关键词：周围神经;损伤;再生;移植;综述文献     

Changes in nerve microcirculation following peripheral nerve compression

Following peripheral nerve compression, peripheral nerve microcirculation plays important roles in regulating the nerve microenvironment and neurotrophic substances, supplying blood and oxygen and maintaining neural conduction and axonal transport. This paper has retrospectively analyzed the articles published in the past 10 years that addressed the relationship between peripheral nerve compression and changes in intraneural microcirculation. In addition, we describe changes in different peripheral nerves, with the aim of providing help for further studies in peripheral nerve microcirculation and understanding its protective mechanism, and exploring new clinical methods for treating peripheral nerve compression from the perspective of neural microcirculation.     

施万细胞在修复外周神经损伤中作用机制的研究进展

外周神经损伤后若不能及时准确的修复,则会导致外周神经功能的永久丧失。目前研究显示施万细胞(SC)参与外周神经损伤后碎片清除、轴突和髓鞘再生以及靶器官再支配过程中,外周神经损伤后SC被迅速激活进入修复过程,经历一系列动态的细胞重塑变化,转化为修复表型,促进神经再生、引导对靶器官再支配,从而恢复神经功能,其中有许多信号通路,转录调节因子等调控这些过程。基于此,该文系统总结了SC在外周神经再生过程中的研究进展,为深入研究外周神经修复提供新的方法和策略。     

Use of nerve conduits for peripheral nerve injury repair A Web of Science-based literature analysis

OBJECTIVE: To identify global research trends in the use of nerve conduits for peripheral nerve injury repair. DATA RETRIEVAL: Numerous basic and clinical studies on nerve conduits for peripheral nerve injury repair were performed between 2002-2011. We performed a bibliometric analysis of the institutions, authors, and hot topics in the field, from the Web of Science, using the key words peripheral nerve and conduit or tube. SELECTION CRITERIA: Inclusion criteria: peer-reviewed published articles on nerve conduits for peripheral nerve injury repair, indexed in the Web of Science; original research articles, reviews, meeting abstracts, proceedings papers, book chapters, editorial material, and news items. Exclusion criteria: articles requiring manual searching or telephone access; documents not published in the public domain; and several corrected papers. MAIN OUTCOME MEASURES: (a) Annual publication output; (b) publication type; (c) publication by research field; (d) publication by journal; (e) publication by funding agency; (f) publication by author; (g) publication by country and institution; (h) publications by institution in China; (i) most-cited papers. RESULTS: A total of 793 publications on the use of nerve conduits for peripheral nerve injury repair were retrieved from the Web of Science between 2002-2011. The number of publications gradually increased over the 10-year study period. Articles constituted the main type of publication. The most prolific journals were Biomaterials, Microsurgery, and Journal of Biomedical Materials Research Part A. The National Natural Science Foundation of China supported 27 papers, more than any other funding agency. Of the 793 publications, almost half came from American and Chinese authors and institutions. CONCLUSION: Nerve conduits have been studied extensively for peripheral nerve regeneration; however, many problems remain in this field, which are difficult for researchers to reach a consensus.     

Craniocerebral injury promotes the repair of peripheral nerve injury

The increase in neurotrophic factors after craniocerebral injury has been shown to promote fracture healing. Moreover, neurotrophic factors play a key role in the regeneration and repair of peripheral nerve. However, whether craniocerebral injury alters the repair of peripheral nerve injuries remains poorly understood. Rat injury models were established by transecting the left sciatic nerve and using a free-fall device to induce craniocerebral injury. Compared with sciatic nerve injury alone after 6–12 weeks, rats with combined sciatic and craniocerebral injuries showed decreased sciatic functional index, increased recovery of gastrocnemius muscle wet weight, recovery of sciatic nerve ganglia and corresponding spinal cord segment neuron morphologies, and increased numbers of horseradish peroxidase-labeled cells. These results indicate that craniocerebral injury promotes the repair of peripheral nerve injury.     

Macrophages contribute to the maintenance of stable regenerating neurites following peripheral nerve injury

Normal adult uninjured nerve is unable to support axonal regeneration. We have studied the mechanisms underlying the regeneration of peripheral nerve by culturing adult mouse dorsal root ganglia (DRG) explants on unfixed, longitudinal cryosections of either the uninjured sciatic nerve or the distal segment of the transected sciatic nerve. We found that, initially, DRG grew vigorously on cryosections of both uninjured and postinjury sciatic nerves. However, the neurites began to degenerate shortly after contact with the uninjured nerve, whereas those growing on postinjury nerve substrate remained healthy for up to 9 days in culture. This ability to support stable outgrowth peaked at 8 days, gradually decreased by 10 days, and disappeared by 20 days after injury. Macrophages appeared in the distal segment by 4 days postinjury and had infiltrated its entire length by 8 days. Uninjured nerve cryosections could be rendered supportive of stable outgrowth by preincubation with macrophage-conditioned medium or by brief trypsinization. The activity of the macrophage-conditioned medium was augmented upon activation of macrophages. Together these findings suggest that the environment of the sciatic nerve undergoes a transformation during Wallerian degeneration such that it becomes transiently supportive of the stable outgrowth of neurites. This transformation may be mediated by a proteolytic activity, generated by activated macrophages, that removes a putative "degeneration signal" protein normally present in the adult nerve and thus contributes to the maintenance of stable regenerating neurites.     

Electrical stimulation accelerates nerve regeneration and functional recovery in delayed peripheral nerve injury in rats

The present study aims to investigate the potential of brief electrical stimulation (ES; 3 V, 20 Hz, 20 min) in improving functional recovery in delayed nerve injury repair (DNIR). The sciatic nerve of Sprague Dawley rats was transected, and the repair of nerve injury was delayed for different time durations (2, 4, 12 and 24 weeks). Brief depolarizing ES was applied to the proximal nerve stump when the transected nerve stumps were bridged with a hollow nerve conduit (5 mm in length) after delayed periods. We found that the diameter and number of regenerated axons, the thickness of myelin sheath, as well as the number of Fluoro‐Gold retrograde‐labeled motoneurons and sensory neurons were significantly increased by ES, suggesting that brief ES to proximal nerve stumps is capable of promoting nerve regeneration in DNIR with different delayed durations, with the longest duration of 24 weeks. In addition, the amplitude of compound muscle action potential (gastrocnemius muscle) and nerve conduction velocity were also enhanced, and gastrocnemius muscle atrophy was partially reversed by brief ES, indicating that brief ES to proximal nerve stump was able to improve functional recovery in DNIR. Furthermore, brief ES was capable of increasing brain‐derived neurotrophic factor (BDNF) expression in the spinal cord in DNIR, suggesting that BDNF‐mediated neurotrophin signaling might be one of the contributing factors to the beneficial effect of brief ES on DNIR. In conclusion, the present findings indicate the potential of using brief ES as a useful method to improve functional recovery for delayed repair of peripheral nerve lesions.     

Role of neuregulin-1 in peripheral nerve injury

Peripheral nerve injury in humans often leads to permanent functional deficits. Schwann cells play an important role in the recovery of peripheral nerve injury by ensheathing axons and providing various neurotrophic factors. Neuregulin-1 (NRG-1) provides axonal signals, which allow dedifferentiation and rapid proliferation of Schwann cells. Subsequently, NRG-1 promotes axonal myelination and influences myelin thickness. Moreover, NRG-1 plays a critical role in synapse formation in the neuromuscular junction. These effects, together, suggest that NRG-1 promotes recovery of peripheral nerve injury.     

Cortical plasticity and nerve regeneration after peripheral nerve injury

With the development of neuroscience, substantial advances have been achieved in peripheral nerve regeneration over the past decades. However, peripheral nerve injury remains a critical public health problem because of the subsequent impairment or absence of sensorimotor function. Uncomfortable complications of peripheral nerve injury, such as chronic pain, can also cause problems for families and society. A number of studies have demonstrated that the proper functioning of the nervous system depends not only on a complete connection from the central nervous system to the surrounding targets at an anatomical level, but also on the continuous bilateral communication between the two. After peripheral nerve injury, the interruption of afferent and efferent signals can cause complex pathophysiological changes, including neurochemical alterations, modifications in the adaptability of excitatory and inhibitory neurons, and the reorganization of somatosensory and motor regions. This review discusses the close relationship between the cerebral cortex and peripheral nerves. We also focus on common therapies for peripheral nerve injury and summarize their potential mechanisms in relation to cortical plasticity. It has been suggested that cortical plasticity may be important for improving functional recovery after peripheral nerve damage. Further understanding of the potential common mechanisms between cortical reorganization and nerve injury will help to elucidate the pathophysiological processes of nerve injury, and may allow for the reduction of adverse consequences during peripheral nerve injury recovery. We also review the role that regulating reorganization mechanisms plays in functional recovery, and conclude with a suggestion to target cortical plasticity along with therapeutic interventions to promote peripheral nerve injury recovery.