Objective:To explore the relationship of peripheral nerve ultrastructure and its associated pro-tein expression in experimental autoimmune neuritis ( EAN) . Methods:EAN was established in Lewis rats using an emulsified mixture of P0 peptide 180-199,Mycobacterium tuberculosis,and incomplete Freund's adjuvant. Rats given saline solution were used as a control group. Sciatic nerve ultrastructure and immunofluorescence histopathol-ogy were measured at the neuromuscular severity peak on day 18 post-induction. Cell-specific protein markers were used for immunofluorescence histopathology staining to characterize sciatic nerve cells:CD3 ( T cell) , Iba-1 ( mi-croglia), S100(myelin), and neurofilament 200(axon). Results:The results showed that swelling of the myelin lamellae, vesicular disorganization,separation of the myelin lamellae, and an attenuation or disappearance of the axon were observed by transmission electron microscopy in the EAN group. CD3 and Iba-1 increased significantly in the structures characterized by separation or swelling of the myelin lamellae,and increased slightly in the struc-tures characterized by vesicular of the myelin lamellae, S100 decreased in the structures characterized by vesicular disorganization or separation of the myelin lamellae. And neurofilament 200 decreased in the structures character-ized by separation of the myelin lamellae. Moreover,we found that Iba1 were positive in the myelin sheath, and o-verlapped with S100 , which significantly indicated that Schwann cells may play as macrophage-like cells during the disease progression of ENA. Our findings may be a significant supplement for the knowledge of EAN model, and may offer a novel sight on the treatment of GBS.

Several studies have demonstrated that L-carnitine exhibits neuroprotective effects on injured sciatic nerve of rats with diabetes mellitus. It is hypothesized that L-carnitine exhibits neuro-protective effects on injured sciatic nerve of rats. Rat sciatic nerve was crush injured by a forceps and exhibited degenerative changes. After intragastric administration of 50 and 100 mg/kg L-carnitine for 30 days, axon area, myelin sheath area, axon diameter, myelin sheath diameter, and numerical density of the myelinated axons of injured sciatic nerve were similar to normal, and the function of injured sciatic nerve also improved signiifcantly. These ifndings suggest that L-carnitine exhibits neuroprotective effects on sciatic nerve crush injury in rats.

Platelet-rich plasma containing various growth factors can promote nerve regeneration. An in-side-out vein graft can substitute nerve autograft to repair short nerve defects. It is hypothesized that an inside-out vein graft iflled with platelet-rich plasma shows better effects in the repair of short sciatic nerve defects. In this study, an inside-out vein autograft iflled with platelet-rich plasma was used to bridge a 10 mm-long sciatic nerve defect in rats. The sciatic nerve function of rats with an inside-out vein autograft iflled with platelet-rich plasma was better improved than that of rats with a simple inside-out vein autograft. At 6 and 8 weeks, the sciatic nerve function of rats with an inside-out vein autograft filled with platelet-rich plasma was better than that of rats undergoing nerve autografting. Compared with the sciatic nerve repaired with a simple inside-out vein autograft, the number of myelinated axons was higher, axon diameter and myelin sheath were greater in the sciatic nerve repaired with an inside-out vein autograft iflled with platelet-rich plasma and they were similar to those in the sciatic nerve repaired with nerve autograft. These findings suggest that an inside-out vein graft filled with platelet-rich plasma can substitute nerve autograft to repair short sciatic nerve defects.

When repairing nerves with adhesives, most researchers place glue directly on the nerve stumps, but this method does not ifx the nerve ends well and allows glue to easily invade the nerve ends. In this study, we established a rat model of completely transected sciatic nerve injury and re-paired it using a modiifed 1 cm-length conduit with inner diameter of 1.5 mm. Each end of the cylindrical conduit contains a short linear channel, while the enclosed central tube protects the nerve ends well. Nerves were repaired with 2-octyl-cyanoacrylate and suture, which complement the function of the modiifed conduit. The results demonstrated that for the same conduit, the av-erage operation time using the adhesive method was much shorter than with the suture method. No signiifcant differences were found between the two groups in sciatic function index, motor evoked potential latency, motor evoked potential amplitude, muscular recovery rate, number of medullated nerve fibers, axon diameter, or medullary sheath thickness. Thus, the adhesive method for repairing nerves using a modiifed conduit is feasible and effective, and reduces the operation time while providing an equivalent repair effect.

Mecobalamin, a form of vitamin B12 containing a central metal element (cobalt), is one of the most important mediators of nervous system function. In the clinic, it is often used to accelerate recovery of peripheral nerves, but its molecular mechanism remains unclear. In the present study, we performed sciatic nerve crush injury in mice, followed by daily intraperitoneal administra-tion of mecobalamin (65 μg/kg or 130 μg/kg) or saline (negative control). Walking track analysis, histomorphological examination, and quantitative real-time PCR showed that mecobalamin signiifcantly improved functional recovery of the sciatic nerve, thickened the myelin sheath in myelinated nerve ifbers, and increased the cross-sectional area of target muscle cells. Further-more, mecobalamin upregulated mRNA expression of growth associated protein 43 in nerve tissue ipsilateral to the injury, and of neurotrophic factors (nerve growth factor, brain-derived nerve growth factor and ciliary neurotrophic factor) in the L4–6 dorsal root ganglia. Our ifndings indicate that the molecular mechanism underlying the therapeutic effect of mecobalamin after sciatic nerve injury involves the upregulation of multiple neurotrophic factor genes.

We have previously shown that Achyranthes bidentata polypeptides (ABPP), isolated from Achy-ranthes bidentata Blume (a medicinal herb), exhibit neurotrophic and neuroprotective effects on the nervous system. To identify the major active component of ABPP, and thus optimize the use of ABPP, we used reverse-phase high performance liquid chromatography to separate ABPP. We ob-tained 12 fractions, among which the fraction of ABPPk demonstrated the strongest neuroactivity. Immunocytochemistry and western blot analysis showed that ABPPk promoted neurite growth in cultured dorsal root ganglion explant and dorsal root ganglion neurons, which might be associated with activation of Erk1/2. A combination of behavioral tests, electrophysiological assessment, and histomorphometric analysis indicated that ABPPk enhanced nerve regeneration and function res-toration in a mouse model of crushed sciatic nerve. All the results suggest that ABPPk, as the key component of ABPP, can be used for peripheral nerve repair to yield better outcomes than ABPP.

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 sciat-ic 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 mor-phologies, and increased numbers of horseradish peroxidase-labeled cells. These results indicate that craniocerebral injury promotes the repair of peripheral nerve injury.

Tensile stress and tensile strain directly affect the quality of nerve regeneration after bridging nerve defects by poly(lactic-co-glycolic acid) conduit transplantation and autogenous nerve grafting for sciatic nerve injury. This study col ected the sciatic nerve from the gluteus maximus muscle from fresh human cadaver, and established 10-mm-long sciatic nerve injury models by removing the ischium, fol owing which poly(lactic-co-glycolic acid) conduits or autogenous nerve grafts were transplanted. Scanning electron microscopy revealed that the axon and myelin sheath were torn, and the vessels of basilar membrane were obstructed in the poly(lactic-co-glycolic acid) con-duit-repaired sciatic nerve fol owing tensile testing. There were no significant differences in tensile tests with autogenous nerve graft-repaired sciatic nerve. Fol owing poly(lactic-co-glycolic acid) conduit transplantation for sciatic nerve repair, tensile test results suggest that maximum tensile load, maximum stress, elastic limit load and elastic limit stress increased compared with autogen-ous nerve grafts, but elastic limit strain and maximum strain decreased. Moreover, the tendencies of stress-strain curves of sciatic nerves were similar after transplantation of poly(lactic-co-glycolic acid) conduits or autogenous nerve grafts. Results showed that after transplantation in vitro for sciatic nerve injury, poly(lactic-co-glycolic acid) conduits exhibited good intensity, elasticity and plasticity, indicating that poly(lactic-co-glycolic acid) conduits are suitable for sciatic nerve injury repair.

The neuropeptides, substance P and calcitonin gene-related peptide, have been shown to be involved in pain transmission and repair of sciatic nerve injury. A model of sciatic nerve defect was prepared by dissecting the sciatic nerve at the middle, left femur in female Sprague Dawley rats. The two ends of the nerve were encased in a silica gel tube. L5 dorsal root ganglia were harvested 7, 14 and 28 days post sciatic nerve injury for immunohistochemical staining. Results showed that substance P and cal-citonin gene-related peptide expression increased significantly in dorsal root ganglion of rats with sci-atic nerve injury. This increase peaked at 7 days, declined at 14 days, and reduced to normal levels by 28 days post injury. The findings indicate that the neuropeptides, substance P and calcitonin gene-related peptide, mainly increased in the early stages after sciatic nerve injury.

It is wel known that peripheral nerve injury should be treated immediately in the clinic, but in some instances, repair can be delayed. This study investigated the effects of immediate versus delayed (3 days after injury) neurorrhaphy on repair of transected sciatic nerve in New Zealand rabbits using stereological, histomorphological and biomechanical methods. At 8 weeks after immediate and de-layed neurorrhaphy, axon number and area in the sciatic nerve, myelin sheath and epineurium thickness, Schwann cellmorphology, and the mechanical property of nerve fibers did not differ ob-viously. These results indicate that delayed neurorrhaphy do not produce any deleterious effect on sciatic nerve repair.

Our previous findings confirmed that the nerve growth factor-containing fibrin glue membrane pro-vides a good microenvironment for peripheral nerve regeneration;however, the precise mechanism remains unclear. p75 neurotrophin receptor (p75NTR) plays an important role in the regulation of pe-ripheral nerve regeneration. We hypothesized that a nerve growth factor-containing fibrin glue membrane can promote neural regeneration by up-regulating p75NTR expression. In this study, we used a silicon nerve conduit to bridge a 15 mm-long sciatic nerve defect and injected a mixture of nerve growth factor and fibrin glue at the anastomotic site of the nerve conduit and the sciatic nerve. Through RT-PCR and western blot analysis, nerve growth factor-containing fibrin glue membrane significantly increased p75NTR mRNA and protein expression in the Schwann cells at the anasto-motic site, in particular at 8 weeks after injection of the nerve growth factor/fibrin glue mixture. These results indicate that nerve growth factor-containing fibrin glue membrane can promote pe-ripheral nerve regeneration by up-regulating p75NTR expression in Schwann cells.

Even though many studies have identified roles of proteasomes in axonal degeneration, the mo-lecular mechanisms by which axonal injury regulates proteasome activity are stil unclear. In the present study, we found evidence indicating that extracellular calcium influx is an upstream regula-tor of proteasome activity during axonal degeneration in injured peripheral nerves. In degenerating axons, the increase in proteasome activity and the degradation of ubiquitinated proteins were sig-nificantly suppressed by extracellular calcium chelation. In addition, electron microscopic findings revealed selective inhibition of neurofilament degradation, but not microtubule depolymerization or mitochondrial swel ing, by the inhibition of calpain and proteasomes. Taken together, our findings suggest that calcium increase and subsequent proteasome activation are an essential initiator of neurofilament degradation in Wal erian degeneration.

Our previous studies have histomorphological y confirmed that nanofibrous poly(3-hydroxybutyrate-co-3-hydroxyvalerate) conduit can be used to repair 30-mm-long sciatic nerve defects. However, the repair effects on rat behaviors remain poorly understood. In this study, we used nanofibrous poly(3-hydroxybutyrate-co-3-hydroxyvalerate) conduit and autologous sciatic nerve to bridge 30-mm-long rat sciatic nerve gaps. Within 4 months after surgery, rat sciatic nerve functional re-covery was evaluated per month by behavioral analyses, including toe out angle, toe spread anal-ysis, walking track analysis, extensor postural thrust, swimming test, open-field analysis and noci-ceptive function. Results showed that rat sciatic nerve functional recovery was similar after nanofibrous poly(3-hydroxybutyrate-co-3-hydroxyvalerate) conduit and autologous nerve grafting. These findings suggest that nanofibrous poly(3-hydroxybutyrate-co-3-hydroxyvalerate) conduit is suitable in use for repair of long-segment sciatic nerve defects.

In this study, we aimed to explore the role of ursolic acid in the neural regeneration of the injured sciatic nerve. BALB/c mice were used to establish models of sciatic nerve injury through unilateral sciatic nerve complete transection and microscopic anastomosis at 0.5 cm below the ischial tuber-osity. The successful y generated model mice were treated with 10, 5, or 2.5 mg/kg ursolic acid via intraperitoneal injection. Enzyme-linked immunosorbent assay results showed that serum S100 protein expression level gradual y increased at 1-4 weeks after sciatic nerve injury, and significantly decreased at 8 weeks. As such, ursolic acid has the capacity to significantly increase S100 protein expression levels. Real-time quantitative PCR showed that S100 mRNA expression in the L 4-6 segments on the injury side was increased after ursolic acid treatment. In addition, the muscular mass index in the soleus muscle was also increased in mice treated with ursolic acid. Toluidine blue staining revealed that the quantity and average diameter of myelinated nerve fibers in the injured sciatic nerve were significantly increased after treatment with ursolic acid. 10 and 5 mg/kg of ursolic acid produced stronger effects than 2.5 mg/kg of ursolic acid. Our findings indicate that ursolic acid can dose-dependently increase S100 expression and promote neural regeneration in BALB/c mice fol owing sciatic nerve injury.

Microsurgical suturing is the gold standard of nerve coaptation. Although literature on the usefulness of ifbrin glue as an alternative is becoming increasingly available, it remains contradic-tory. Furthermore, no data exist on how both repair methods might inlfuence the morphological aspects (arborization; branching) of early peripheral nerve regeneration. We used the sciatic nerve transplantation model in thy-1 yellow lfuorescent protein mice (YFP;n = 10). Pieces of nerve (1cm) were grafted from YFP-negative mice (n = 10) into those expressing YFP. We per-formed microsuture coaptations on one side and used ifbrin glue for repair on the contralateral side. Seven days after grafting, the regeneration distance, the percentage of regenerating and ar-borizing axons, the number of branches per axon, the coaptation failure rate, the gap size at the repair site and the time needed for surgical repair were all investigated. Fibrin glue repair resulted in regenerating axons travelling further into the distal nerve. It also increased the percentage of arborizing axons. No coaptation failure was detected. Gap sizes were comparable in both groups. Fibrin glue signiifcantly reduced surgical repair time. The increase in regeneration distance, even after the short period of time, is in line with the results of others that showed faster axonal regen-eration after ifbrin glue repair. The increase in arborizing axons could be another explanation for better functional and electrophysiological results after ifbrin glue repair. Fibrin glue nerve coap-tation seems to be a promising alternative to microsuture repair.

晚期周围神经损伤后感觉功能恢复中:脊髓后角P物质及降钙素基因相关肽的变化

背景:晚期周围神经损伤有无修复价值?如果脊髓神经元中P物质和降钙素基因相关肽的变化发生了不可逆的变化,其修复后也预示着感觉功能的缺失. 目的:定量研究周围神经损伤24周后,脊髓后角中P物质和降钙素基因相关肽的变化.设计:建立以大鼠坐骨神经损伤为研究对象的实验模型,损伤后24周为远期观察点,自身对照(对侧空白组),定量化研究.单位:第四军医大学骨科研究所.材料:实验于2002-10/2003-05在第四军医大学骨科研究所完成.SD大鼠55只,分成11组,即坐骨神经切断1,2,3,4,6,8,10,12,16,20,24周各组.干预:切断大鼠一侧坐骨神经并结扎其近端的方法建立周围神经损伤模型;另一侧为对照侧.应用计算机图像分析技术测试P物质和降钙素基因相关肽免疫反应区的面积.主要观察指标:各组大鼠脊髓后角中P物质和降钙素基因相关肽阳性纤维的终末分布面积的变化.结果:55只大鼠均进入结果分析.①P物质时间序列表示:周围神经损伤后2～6周,P物质在脊髓后角免疫反应区面积下降至低,随之回升,至16周恢复正常,20,24周无明显的进一步变化.②脊髓后角降钙素基因相关肽阳性纤维和终末分布面积损伤与自身对照侧的比值:1周时1.14,6周时1.13,24周时0.29,各时间点基本相似(P＞0.05)结论:周围神经损伤至晚期,脊髓后角及后根神经节细胞合成和分泌P物质及降钙素基因相关肽的功能尚未受到破坏,脊髓后角已处于一种稳定的平衡状态,仍有恢复感觉功能的神经学基础.

下背部痛:急性下背痛

Pain in the low lumbar, lumbosacral, or sacroiliac region, possibly accompanied by pain radiating down one or both buttocks or legs in the distribution of the sciatic nerve (sciatica).

小儿注射性臀肌挛缩症的手术治疗

本文报告手术治疗300余例臀肌挛缩症的经验教训和71例随诊结果.此症确诊后应及早手术治疗.手术要求切断所有妨碍髋屈曲、内收和内旋的挛缩组织,松解彻底,注意避免损伤坐骨神经.术后两下肢靠拢,布带松松固定,避免两髋外展.术后第3天起可逐渐活动两下肢.71例术后随访6个月～3年5个月,其中64例疗效满意,7例活动功能改善.

Bilateral hip dislocation rarely occurs.In this paper, a case of bilateral hip dislocation associated with bilateral sciatic nerve palsy resulted from a road traffic acci-dent is reported.Both hips were emergently reduced under general anaesthesia.Acetabular reconstruction was done bilaterally due to the unstable hips.The patient subsequently developed heterotopic ossification and avascular necrosis on the left hip and underwent total hip arthroplasty.The sciatic nerve on the right side achieved complete recovery but that on the left side only partly recovered and was aug-mented by tendon transfer.Such injuries are serious and one should be aware of the complications because they can resurface and so patients should be followed up for a long time.To the best of our knowledge, this kind of injury has not been reported in the English .language literature.