干细胞及神经相关因子对运动性周围神经损伤再生的影响

背景：当前干细胞技术在心脑血管病、中枢神经损伤和外周神经损伤等都具有十分重要的作用。但是在对运动引起周围神经损伤方面的研究还处于基础阶段。 目的：论文旨在研究当前干细胞技术运用于运动性周围神经损伤的研究现状,为运动性周围神经损伤的康复奠定科学基础。 方法：通过计算机检索PubMed数据库1991-01/2010-01的相关文献,文献所述内容与干细胞和运动性周围神经损伤的研究密切相关。共选取26篇文献, 结果与结论：运动训练中经常出现所谓的周围神经损伤性疾病,而依靠干细胞移植和诱导分化技术可以促进周围神经损伤的再生,且对促进运动训练中周围神经损伤的防治具有十分重要的作用。但由于目前尚处于基础研究阶段,还有待进一步的深入研究。     

上肢周围神经修复后手部功能的康复训练体会

周围神经损伤后,常有不同程度的运动、感觉障碍,比如桡神经损伤呈垂腕、垂指,正中神经损伤呈“猿手”畸形;尺神经损伤呈“爪指”畸形等。2002-12～2004-02我们对37例上肢神经损伤后的患者进行了系统有序的促进功能康复的各种护理,获得了满意的效果。现报道如下。1临床资料本组病人37例,男28例,女9例,年龄4.5～63岁。损伤神经:桡神经损伤18例(儿童6例),正中神经12例(儿童2例),尺神经6例,腋神经1例。损伤原因:玻璃割伤16例刀砍伤10例,压迫缺血性损伤4例,钝性损伤6例,电击伤1例。2功能康复护理2.1心理护理上肢周围神经损伤后造成手功能障碍,病…     

周围神经损伤修复及功能恢复评价

摘要 目的：评价修复周围神经缺损的各种生物型人工材料的性能、应用以及功能恢复评定方法,寻找适宜的周围神经替代物。 方法：以“神经导管,周围神经损伤修复,生物材料,许旺细胞”为关键词,采用计算机检索2004-01/2010-11相关文章。纳入与生物材料以及组织工程神经相关的文章;排除重复研究或Meta分析类文章。以28篇文献为主,重点讨论周围神经修复生物型人工材料的种类、性能以及适宜的功能恢复评定方法。 结果：以脱细胞神经基质以及人工合成可降解材料为主体的复合型生物工程材料可作为较理想的支架材料应用于周围神经组织工程。脱细胞神经支架解决了自体神经来源受限、移植物排斥反应等问题,韧性与可塑性接近自体神经,微环境更利于周围神经再生。人工合成可降解材料具有生物降解、可塑性、一定的通透性等优势,且已有商品化成品出现。若将上述材料分别合理构建复合材料,有可能得到性能良好的组织工程神经移植物。周围神经修复后功能恢复评定方法主要以大体与形态学观察、组织学、神经肌肉机能学评定为主,辅以分子生物学技术。各类评定方法的应用有利于筛选出最适宜的周围神经损伤修复材料与构建方案。 结论：周围神经损伤修复生物型人工材料研究发展迅速,但仍没有超越自体神经移植的支架材料。脱细胞神经基质以及人工合成可降解材料复合构建支架可作为较好的周围神经支架,但仍需要与种子细胞、神经营养因子等联合构建,以取得良好的促进再生效果。当前,对周围神经损伤修复效果的评定更加注重于神经肌肉功能的恢复,迫切需要筛选出最佳的修复材料以及构建方案以满足组织工程神经移植以及功能康复的要求,达到对周围神经损伤后形态、结构修复与功能重建的目的。 关键词：神经组织工程;周围神经;功能恢复;生物型人工材料;神经移植物 doi:10.3969/j.issn.1673-8225.2011.08.030     

神经导引管与周围神经再生

周围神经损伤后神经缺损的临床治疗效果不能令人满意。应用人工合成材料制成的神经导引管桥接两神经断端可以促进神经再生 ,再生神经的运动感觉功能恢复满意 ,这种导管具有许多优点 ,被许多学者推荐为替代直接缝合和自体神经移植治疗周围神经损伤的一个理想方法。     

白血病抑制因子在周围神经损伤修复中的应用

神经营养因子在周围神经损伤中的应用,是当前的一个研究热点。白血病抑制因子(LIF)是一种对感觉、运动和自主神经元都敏感的神经营养因子,周围神经损伤后其在损伤处的表达上调且逆行运输至神经元胞体的量增加,通过与相应受体结合后,起着维持损伤后神经元的存活;促进神经轴突的生长;参与神经损伤后的炎性反应;调节神经元基因和多种神经肽的表达;促进其它神经营养因子的分泌等生物效应,在周围神经修复再生过程的多个方面中起着重要的作用。     

周围神经放射性损伤的研究进展

颈部肿瘤、乳腺癌及盆腔肿瘤放疗后长期生存的病人均会出现不同程度的放射性周围神经病变。周围神经损伤的阈值为20Gy～25Gy,其波动与加用其他治疗方式有关,在高剂量时其形态学变化主要表现为神经轴突和髓鞘的变性坏死;而在低剂量时可观察到神经内膜、神经外膜等的纤维化、神经周围血管的损伤,电镜下可观察到神经微丝微管的聚集,为神经轴突运输障碍和能量生成障碍的表现。目前关于周围神经损伤修复的研究主要是关于外伤所致周围神经损伤的修复,其研究结果是否适用于放射性损伤尚有待研究。     

肌电诱发电位仪联合康复训练治疗外伤性周围神经损伤

目的探讨肌电图动态监测在外伤所致周围神经损伤电刺激联合康复治疗中的临床价值。方法 86例外伤所致周围神经损伤患儿,随机分为治疗组43例和对照组43例,治疗组给予肌电图定位定量电刺激联合康复治疗,对照组给予低频电脉冲治疗联合康复治疗,在肌电图仪的持续监测下分析2组相应神经在刺激前后的电学变化。结果治疗组桡神经传导速度、正中神经的传导速度、尺神经的传导速度均明显高于对照组和治疗前。2组运动电位潜伏期明显缩短,波幅增大;治疗组治疗效果明显优于对照组。结论外伤所致周围神经损伤患儿应用肌电图仪的定位定量电刺激治疗效果明显,能有效促进周围神经再生及神经功能恢复,值得临床推广使用。     

慢性特发性轴索性周围神经病

慢性特发性轴索性周围神经病(chron ic id iopath ic axonalpolyneuropathy,C IAP)是于50岁以后发病的一种原因不明的慢性轴索性周围神经病[1],多为隐袭起病,出现缓慢进展的感觉或感觉运动性周围神经病变症状,神经电生理特点为周围神经轴索性损害。病理检查证实周围神经以轴索损害为主,伴随或不伴随髓鞘损害。自从1993年由Noterm ans等[1]提出该诊断后,在发病机制以及诊断和鉴别诊断等方面存在诸多争议。一些遗传性、慢性炎症性和中毒性轴索性周围神经病常归于C IAP的范畴[2,3]。我们对C IAP在病因、临床、电生理、诊断和治疗等方面的…     

神经干细胞与运动性神经疾病

背景：神经干细胞以其所具有的多向分化潜能、自我更新、迁徙性、低免疫性等特点受到临床的广泛应用，但有关神经干细胞在运动医学领域用于防治运动性损伤等的研究成果不是很多。 目的：旨在通过分析神经干细胞的生物学特性，探讨其在临床上的应用，为神经性疾病的预防和治疗提供理论依据。 方法：应用计算机检索CNKI和PubMed数据库中1997-01/2010-10关于神经干细胞与运动性神经疾病的文章，在标题和摘要中以“神经干细胞，运动医学，失神经肌萎缩，周围神经损伤”或“Neural Stem Cell，Sports Medicine，Denervation Muscle Atrophy，Peripheral Nerve Injury”为检索词进行检索，选择文章内容与神经干细胞和运动性神经疾病相关，同一领域文献选择近期发表或发表在权威杂志上的文章，初检得到262篇文献，根据纳入标准选择31篇进行综述。 结果与结论：神经干细胞以其多向分化潜能、自我维持和更新、低免疫原性、迁徙性和来源广泛等特点为其在治疗神经退行性病变、运动性骨骼肌失神经肌萎缩和促运动性周围神经损伤的再生等提供了较为广阔的应用前景，但由于基础性研究所限，对其作用机制、诱导分化、迁移等仍有待大量的实验研究予以证实。     

周围神经的诱导修复

在外伤性的损伤中约有2.8%的人造成周围神经的损伤(如车祸和工伤等),而其中65%的人伤势严重,而且他们大多数年龄在18～35周岁的青壮年男子,损伤后的周围神经需要在一定的时间内进行修复和重建,否则损伤神经所支配的器官或组织的功能将丧失.在周围神经的损伤中除了外伤性损伤外,还有自发性损伤、医源性损伤、压迫性综合征和系统性疾病等,而这些神经损伤或病变中诸多是显微外科所不能治愈的,神经的诱导修复和再生是最好的解决办法.目前周围神经的修复和再生的标准方法是自体神经移植(Autologous nerve graft, ANG),但是由于能够提供自体神经移植的捐赠部位十分有限,远远不能满足需要,有些较长或粗大的周围神经损伤不是一两个捐赠部位的神经所能解决的,而且捐赠部位的神经的损伤会造成新的功能的丧失.因此许多学者利用异体材料或人工合成材料来诱导周围神经的修复和再生进行了大量的研究,希望能够取代自体神经移植.本文就近几年的基质材料的选择、许旺细胞(Schwann cells,SCs)、生长因子和生物学评价等方面的进展作一综述.     

Nerve growth factor and injured peripheral nerve regeneration

Nerve growth factor （NGF） exhibits many biological activities, such as supply of nutrients, neuroprotection, and the generation and rehabilitation of injured nerves. The neuroprotective and neurotrophic qualities of NGF are generally recognized. NGF may enhance axonal regeneration and myelination of peripheral nerves, as well as cooperatively promote functional recovery of injured nerves and limbs. The clinical efficacy of NGF and its therapeutic potentials are reviewed here. This paper also reviews the latest NGF research developments for repairing injured peripheral nerve, thereby providing scientific evidence for the appropriate clinical application of NGF.     

Bacterial melanin promotes recovery after sciatic nerve injury in rats

Bacterial melanin, obtained from the mutant strain of Bacillus Thuringiensis, has been shown to promote recovery after central nervous system injury. It is hypothesized, in this study, that bacterial melanin can promote structural and functional recovery after peripheral nerve injury. Rats subjected to sciatic nerve transection were intramuscularly administered bacterial melanin. The sciatic nerve transected rats that did not receive intramuscular administration of bacterial melanin served as controls. Behavior tests showed that compared to control rats, the time taken for instrumental conditioned reflex recovery was significantly shorter and the ability to keep the balance on the rotating bar was significantly better in bacterial melanin-treated rats. Histomorphological tests showed that bacterial melanin promoted axon regeneration after sciatic nerve injury. These findings suggest that bacterial melanin exhibits neuroprotective effects on injured sciatic nerve, contributes to limb motor function recovery, and therefore can be used for rehabilitation treatment of peripheral nerve injury.     

Functional reconstruction following brachial plexus root avulsion

OBJECTIVE: To sum up the treatment of brachial plexus root avulsion and the progress in functional reconstruction and rehabilitation following brachial plexus root avulsion. DATA SOURCES: A search of Medline was performed to select functional reconstruction and rehabilitation following brachial plexus injury-related English articles published between January 1990 and July 2006, with key words of "brachial plexus injury, reconstruction and rehabilitation". Meanwhile, a computer-based search of CBM was carried out to select the similar Chinese articles published between January 1998 and July 2006, with key words of "brachial plexus injury, reconstruction and rehabilitation". STUDY SELECTION: The materials were checked primarily, and the literatures of functional reconstruction and rehabilitation of brachial plexus injury were selected and the full texts were retrieved. Inclusive criteria: ① Functional reconstruction following brachial plexus injury. ② Rehabilitation method of brachial plexus injury. Exclusive criteria: Reviews, repetitive study, and Meta analytical papers. DATA EXTRACTION: Forty-six literatures about functional reconstruction following brachial plexus injury were collected, and 36 of them met the inclusive criteria. DATA SYNTHESIS: Brachial plexus injury causes the complete or incomplete palsy of muscle of upper extremity. The treatment of brachial plexus is to displace not very important nerves to the distal end of very important nerve, called nerve transfer, which is an important method to treat brachial plexus injury. Postoperative rehabilitations consist of sensory training and motor functional training. It is very important to keep the initiativeness of exercise. Besides recovering peripheral nerve continuity by operation, combined treatment and accelerating neural regeneration, active motors of cerebral cortex is also the important factor to reconstruct peripheral nerve function. CONCLUSION: Consciously and actively strengthening functional exercise after operation is helpful to form cerebral plasticity and produce voluntary movements, can re-educate re-dominated muscle, obviously improves postoperative therapeutic effect and promote functional reconstruction.     

Effects of forced,passive, and voluntary exercise on spinal motoneurons changes after peripheral nerve injury

After peripheral nerve injury, there are important changes at the spinal level that can lead to disorganization of the central circuitry and thus compromise functional recovery even if axons are able to successfully regenerate and reinnervate their target organs. Physical rehabilitation is a promising strategy to modulate these plastic changes and thus to improve functional recovery after the damage of the nervous system. Forced exercise in a treadmill is able to partially reverse the synaptic stripping and the loss of perineuronal nets that motoneurons suffer after peripheral nerve injury in animal models. The aim of this study was to investigate whether passive exercise, by means of cycling in a motorized bicycle, or voluntary free running in a wheel is able to mimic the effects induced by forced exercise on the changes that axotomized motoneurons suffer after peripheral nerve injury. Partial preservation of synapses and perineuronal nets was observed only in axotomized motoneurons from animals subjected to high‐intensity cycling and the ones that freely ran long distances, but not when low‐intensity exercise protocols were applied. Therefore, the intensity but not the type of exercise used is the key element to prevent synaptic stripping and loss of perineuronal nets in motoneurons after axotomy.     

Peripheral nerve injury and myelination: Potential therapeutic strategies

Traumatic peripheral nerve injury represents a major clinical and public health problem that often leads to significant functional impairment and permanent disability. Despite modern diagnostic procedures and advanced microsurgical techniques, functional recovery after peripheral nerve repair is often unsatisfactory. Therefore, there is an unmet need for new therapeutic or adjunctive strategies to promote the functional recovery in nerve injury patients. In contrast to the central nervous system, Schwann cells in the peripheral nervous system play a pivotal role in several aspects of nerve repair such as degeneration, remyelination, and axonal growth. Several non-surgical approaches, including pharmacological, electrical, cell-based, and laser therapies, have been employed to promote myelination and enhance functional recovery after peripheral nerve injury. This review will succinctly discuss the potential therapeutic strategies in the context of myelination following peripheral neurotrauma.     

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.     

The influence of trkB deficiency on long-term outcome of peripheral nerve injury in mice

The long-term outcome of peripheral nerve injury is often unsatisfactory, especially if the injury resulted in a gap between transected nerve stumps. Brain-derived neurotrophic factor and its receptor, trkB, are strongly implicated in the early phase of axonal regeneration after injury. We examined the role of trkB in long-term functional and morphological outcome of peripheral nerve injury. The sciatic nerve was transected in wild-type and heterozygous trkB-deficient mice. The nerve was either left cut or immediately sewn up or the gap injury model was performed. The gap was provided with autologous or cross (obtained from other genetic group) graft. Sciatic nerve function as well as autotomy was assessed during 16-week follow-up. The long-term functional outcome of nerve cut or immediately rejoined did not differ between wild-type and trkB-deficient mice. Gap injury provided with nerve graft resulted in better functional outcome in trkB-deficient mice than wild-type animals. Sixteen weeks after the surgery, the animals were sacrificed and histological evaluations were performed. The number of nerve fibres regenerating into the distal stump of transected and rejoined nerves did not differ between wild-type and trkB-deficient animals. TrkB deficiency markedly increased the number of Schwann cells as well as mast cells at the injury site and in the distal stump of the regenerating nerve. TrkB deficient nerves also showed higher expression of bcl-2 protein but lower of trkA and NGF than wild-type ones. Our results show for the first time the possible deleterious role of trkB receptor in long-term outcome of peripheral nerve injury.     

Focal and generalized peripheral nerve dysfunction in spinal cord-injured patients.

SUMMARY: The present study was undertaken to quantitate the incidence and clinical patterns of peripheral nerve dysfunction distal to the level of injury in patients with spinal cord injury (SCI). Through retrospective analysis, SCI patients were identified after referral for neurophysiologic investigation of new neuropathic symptoms. In total, peripheral nerve or nerve root lesions developed in 34 SCI patients, most commonly within the first year after SCI. Carpal tunnel syndrome was the most common upper-limb neuropathy (34%); sciatic neuropathy was the most common lower-limb abnormality (8.5%). A significant proportion of SCI patients had neurophysiological evidence of generalized peripheral nerve dysfunction, specifically axonal neuropathy (18%). Tetraplegic patients developed more frequent peripheral nerve lesions than paraplegics. Although most SCI patients presented within 4 years of their original injury, in a more chronic population of SCI patients that developed neuropathy 5 years after injury, 60% had evidence of coexistent syrinx formation. Maintenance of peripheral nerve function is a critical issue in all acute SCI and rehabilitation units, particularly in the context of spinal cord neuronal regeneration projects.