Objective To explore effects of several immunosuppressants on cytokine expressions after repair for a sciatic nerve injury in a rat model. Methods The sciatic nerves of 42 rats were cut and suturedend to end. After operation, the rats were divided into 6 groups. Group A(n=9) was served as a control with no medicines given. Group B (n=9) was given methylprednisolone 20 mg/(kg·d) for 2 days. Groups C(n=9) and D(n=3) were given FK506 1 mg/(kg·d) for 2 weeks and 4 weeks respectively, and were given the same doses of methylprednisolone as Group B. Groups E and F were given CsA 2 mg/(kg·d) for 2 weeks and 4 weeks respectively, and were given the same doses of methylprednisolone as Group B. The sciaticnerves were sampled at 1, 2 and 4 weeks postoperatively. And immuneohistochemistry stainings of interleukin 1β(IL-1β)， tumor necrosis factor α(TNF-α), interferon γ(IFN-γ) and macrophage migration inhibitory factor(MIF) were performed. The staining results were compared and analyzed. Results The expression peaks of IL-1β and IFN-γ were found at the 1st week postoperatively in Group A. Then, the expression decreased rapidly at the 2nd week and disappeared at the 4th week. As for TNF-α and MIF, they were only found to have a low expression until the 1st week in Group A. In groups C-F, the expression peaks of IL-1β, TNF-α and IFN-γ were found at the 2nd week, while the expression peak of MIF was still at the 1st week, and the expression of all the cytokines extended to the 4th week. The expressions of these cytokines in Group B were just between the expression levels of Group A and Groups C-F. Conclusion Immunosuppressants can delay the expression peaks and significantly extend the expression time of IL-1β, TNF-α, IFN-γ and MIF after repair for a sciatic nerve injury in a rat model.
Ten, fifteen and twenty millimeter nerve defects were produced on both trunks of sciatic nerve in 18 rabbits. The stumps of the nerve were enclosed by a silicon tube in the right hind limb (slilcon group) and the left limbs were free (free group). The proximal and distal nerve stumps in both groups were elongated by using a selfdesigned nerve stretching device, and the nerve were gradually stretched by 1mm, 2mm and 3mm per day respectively. when the expected lengths were achieved, the defects of the nerve were managed by endtoend coaptation. The samples were analysed by electrophysiological examination, and light and electron microscopes. Results were as follows: (1) The nerve defect could be repaired by gradual elongation in rabbits; (2) The results of silicon group were superior to the free group; (3) The structure and microcirculation of the nerve would be damaged if the stretching speed exceeded the limit of 2mm per day. But the eventual results following repair by elongation could not reached the normal level.
OBJECTIVE Following the delayed repair of peripheral nerve injury, the cell number of anterior horn of the spinal cord and its ultrastructural changes, motorneuron and its electrophysiological changes were investigated. METHODS In 16 rabbits the common peroneal nerves of both sides being transected one year later were divided into four groups randomly: the degeneration group and regeneration of 1, 3 and 5 months groups. Another 4 rabbits were used for control. All transected common peroneal nerves underwent epineural suture except for the degeneration group the electrophysiological examination was carried out at 1, 3 and 5 months postoperatively. Retrograde labelling of the anterior horn cells was demonstrated and the cells were observed under light and electronmicroscope. RESULTS 1. The number of labelled anterior horn cell in the spinal cord was 45% of the normal population after denervation for one year (P lt; 0.01). The number of labelled cells increased steadily from 48% to 57% and 68% of normal values at 1, 3 and 5 months following delayed nerve repair (P lt; 0.01). 2. The ultrastructure of the anterior horn cells of the recover gradually after repair. 3. With the progress of regeneration the latency become shortened, the conduction velocity was increased, the amplitude of action potential was increased. CONCLUSION Following delayed repair of injury of peripheral nerve, the morphology of anterior horn cells of spinal cord and electrophysiological display all revealed evidence of regeneration, thus the late repair of injury of peripheral nerve was valid.
Objective To investigate the latest development in diagnosis and treatment of the injury to the peripheral nerve. Methods The literature at home and abroad was reviewed, and the research findings with clinical experience in diagnosis and treatment for the injury to the peripheral nerve were summarized. Results The treatment for the total brachial plexus avulsion injury was successfully performed by the extra-plexus nerve transfer. The avulsion of the brachial plexus could be directly repaired by the healthy C7 nerve root transfer through the anterior spinal approach. The forearm flexors could bereinforced by the neurovascularized gracilis transplantation. MRI and CTM werethe best methods of early diagnosis for the brachial plexus injury. The pure upper or lower root avulsion of the brachial plexus injuries could be repaired by the intraplexus nerve transfer, which involved a transfer of part of the ulnarnerve in the arm to the motor nerve of the biceps for C5-C6 avulsion of the brachial plexus,and a transfer of selective fascicles of the healthy C7 nerve root or brachial muscle branch to the flexors muscle fascicles of the median nerve or anterior interosseous nerve. The thoracic outlet syndrome always occurred in this position when the neck muscle fatigue occurred in the typists or the gameplayers after their longstanding looking forwards. The C5 and C6 rootswere rolled by the tendenofibrotic tissue at the origin of the scalenus. After a procain block, the symptom subsided. Radiation neuropathy was a series of pathological changes caused by overdoses of the radiation therapy. The pathologic findings consisted of a series of vessel damages and final coagulation necrosis, which induced clusters of abnormally-dilated, thin-walled telangiectasias. Radiation neuropathy could be detected by MRI and could be differentiated from tumor. Once the diagnosis was established, the therapy should be begun early, including the systemic use of steroids, anticoagulation, and hyperbaric oxygen. Conclusion Great progress has been made in diagnosis and treatment of the injury to the peripheral nerve, but a further study should be performed topromote regeneration of the nerves and reconstruction of the related functions.
In order to investigate the causes, diagnosis, treatment, outcome and prevention of iatrogenic nerve injury in the neck, 8 cases with iatrogenic nerve injuries were analyzed. Among them, 5 cases were accessory nerve injury, 3 cases were brachial plexus injury. All of the cases were treated by surgical methods, including neurolysis, repair by direct suture, nerve graft and transposition. After 1-3 years follow up the effect was excellent in 2 cases who were accessory nerve injury, good in 5 cases, and poor in 1 case who was brachial plexus injury. It was concluded that high responsibility of surgeons and careful manipulation during operation were the key to prevention of nerve injuries.
Objective Peri pheral nerve injury is a common cl inical disease, to study the effects of the physical therapy on the regeneration of the injured sciatic nerve, and provide a reference for cl inical treatment. Methods Sixty-four female adult Wistar rats (weighing 252-365 g) were chosen and randomly divided into 4 groups (n=16): group A, group B, groupC, and group D. The experimental model of sciatic nerve defect was establ ished by crushing the right sciatic nerve in groups B, C, and D; group A served as the control group without crushing. At 2 days after injury, no treatment was given in group B, electrical stimulation in group C, and combined physical therapies (decimeter and infrared ray) in group D. At 0, 7, 14, and 30 days after treatment, the sciatic nerve function index (SFI) and the motor nerve conduction velocity (MNCV) were measured, and morphological and transmission electron microscopy (TEM) examinations were done; at 30 days after treatment, the morphological evaluation analysis of axons was performed. Results At 0 and 7 days after treatment, the SFI values of groups B, C, and D were significantly higher than that of group A (P lt; 0.05); at 14 and 30 days after treatment, the SFI value of group D decreased significantly, no significant difference was observed between group D and group A (P gt; 0.05) at 30 days; whereas the SFI values of groups B and C decreased, showing significant difference when compared with the value of group A (P lt; 0.05). At 0, 7, and 14 days after treatment, the MNCV values of groups B, C, and D were significantly lower than that of group A (P lt; 0.05), and there were significantly differences between group B and groups C, D (P lt; 0.05); at 14 days, the MNCV value of group D was significantly higher than that of group C (P lt; 0.05); and at 30 days, the MNCV values of groups B and C were significantly lower than that of group A (P lt; 0.05), but there was no significant difference between group D and group A (P gt; 0.05). At 0 and 7 days, only collagen and l i pid were observed by TEM; at 14 and 30 days, many Schwann cells and perineurial cells in regeneration axon were observed in groups B, C, and D, especially in group D. Automated image analysis of axons showed that there was no significant difference in the number of myelinated nerve fibers, axon diameter, and myelin sheath thickness between group D and group A (P gt; 0.05), and the number of myelinated nerve fibers and axon diameter of group D were significantly higher than those of groups B and C (P lt; 0.05). Conclusion Physical therapy can improve the regeneration of the injured sciatic nerve of rats.
Objective To review the progress and application of peripheral nervous microelectrode. Methods The recent articles on peripheral nervous microelectrode were extensively reviewed. The classification, the progress of the peripheral nervous microelectrode and its utilizable prospect in the control of electronic prosthesis were summarized. Results The microelectrodes had favorable functions of selective stimulation and recording. It provided an information transmitting interface between the electric prosthesis and peripheral nerves. Conclusion Peripheral nervous signal is a feasible signal source to control electronic prosthesis.
To find new technique for repair of peripheral nerve defect, the nerve elongation repair technique was adopted. Two cases with nerve defect were treated by this method. One was a 12 year old male, the defect length of right radial nerve was 7.2 cm at the elbow. The other one was a 28 year old male, the defect length of left ulnar nerve the was 5 cm at elbow. In this method, the nerve was elongated by slow stretch from distal and proximal end of the ruptured nerve. After a few days, the nerve was repaired by direct suture. After operation, the function of nerves were recovered in 119 days and 114 days respectively. Follow-up for 5 years, the function of the effected limbs were recovered to the normal side. It was concluded that: (1) the peripheral never can be elongated by slow stretch; (2) to stretch the nerve end in a rubber tube can prevent adhesion and connective tissue blocking; (3) strength and supporting point of stretching should be designed carefully.
OBJECTIVE: To explore the possibility to bridge peripheral nerve defects by xenogeneic acellular nerve basal lamina scaffolds. METHODS: Thirty SD rats were randomly divided into 5 groups; in each group, the left sciatic nerves were bridged respectively by predegenerated or fresh xenogeneic acellular nerve basal lamina scaffolds, autogenous nerve grafting, fresh xenogeneic nerve grafting or without bridging. Two kinds of acellular nerve basal lamina scaffolds, extracted by 3% Triton X-100 and 4% deoxycholate sodium from either fresh rabbit tibial nerves or predegenerated ones for 2 weeks, were transplanted to bridge 15 mm rat sciatic nerve gaps. Six months after the grafting, the recovery of function was evaluated by gait analysis, pinch test, morphological and morphometric analysis. RESULTS: The sciatic nerve function indexes (SFI) were -30.7% +/- 6.8% in rats treated with xenogeneic acellular nerve, -36.2% +/- 9.7% with xenogeneic predegenerated acellular nerve, and -33.9% +/- 11.3% with autograft respectively (P gt; 0.05). The number of regenerative myelinated axons, diameter of myelinated fibers and thickness of myelin sheath in acellular xenograft were satisfactory when compared with that in autograft. Regenerated microfascicles distributed in the center of degenerated and acellular nerve group. The regenerated nerve fibers had normal morphological and structural characters under transmission electron microscope. The number and diameter of myelinated fibers in degenerated accellular nerve group was similar to that of autograft group (P gt; 0.05). Whereas the thickness of myelin sheath in degenerated accellular nerve group was significantly less than that of autograft group (P lt; 0.05). CONCLUSION: The above results indicate that xenogeneic acellular nerve basal lamina scaffolds extracted by chemical procedure can be successfully used to repair nerve defects without any immunosuppressants.
Basing on the experimental results, 48 nerve defects (with the length of 3-4 cm in 21 cases, 4.1-5cm in 25 cases and 6cm in 2 cases) were repaired clinically by using vaseularized nerve sheath canal with living Schwann s cells, 87.5 percent of them obtained good results. The advantages were: (1) The neural sheath had rich blood supply with resultant less scar from its healing; (2) The living Schwann s cells would secrete somatomedin to promote the reproduction of neural tissues; and (3) The useless neurofib...