Nine cases of sciatic nerve from injection hadbeen treated by fasciotomy. The skin temperatureof the diseased limb immediately raised 1-2℃ fol-lowing operation. The cutaneous sensation began torecover 2-3 days after operation. Two cases ofplantar ulcer recovered one month post operation.Five of the eight cases of paralysis of muscle in-nervated by the common peroneal nerve recoveredto normal. The etiology,pathology, and therapeuticmethods of the nerve injury caused by drug injec-tion were discused.
Abstract In case of sciatic nerve injury, there is degeneration of neuron in the corresponding segment of spinal cord. To study whether NGF could protect the dorsal root ganglia in this situation, the following experiments were performed: 72 SD mice were divided into 2 groups. In each mouse, the sciatic nerve was sectioned at the middle of the right thigh, and then,the proximal end of the sciatic nerve was inserted into a one ended silastic tube. The NGF 0.15ml (contain 2.5S NGF 0.15mg) was injected into the tubes of the experimental group, while a equal amount of normal saline was injected into the tubes of the control group. After 1, 3, 5, 9, 20 and 30 days, 6 mice of each groupwere sacrificed respectively, and 5th to 6th lumbar segments of the spinal cords were resected for examination. By histochemical study, the activity of fluoride resistant acid phosphatase (FRAP) of each animal was detected. The results showed: (1) Excision of the sciatic nerve led to decrease of FRAP activity, it suggested that the injury of sciatic nerve could damage the dorsal root ganglia; (2) The use of exogenous NGF could protect the FRAP activity. It was concluded that NGF played an important role in protecting the dorsal root ganglia in peripheral nerve injury, in vivo.
Objective To make a histological evaluation of poly(dextrogyr-levogyr)lactide acide-triiodothy-ronine (PDLLA-T3) in sciatic nerve defect of rat. Methods Ninety SD rats were evenly divided into 3 groups (autograft group A, PDLLA-T3 group B and PDLLA group C). Group D was control group. The left sciatic nerves were cut off by operation and 1 cm-nerve-defect was set up. The specimens were collected 2 weeks,1 month and 2 months after the operation respectively, simultaneously the right sciatic nerves were collected as normal control group D. HE stainning, electron microscope, S100 immunohistochemistry, and Bielschowsky staining were done in all the specimens, the quantity and quality of the regenerated nerves were observed, and all the results were processed by image analyzer.Results Two weeks after the operation,histological observation indicated that the materials in groups B and C were not completely degraded. Transmission electron microscopic observationshowed that the myelin sheath was not thick and it was about 0.5 μm in thickness. There was no significant difference among the 3 groups. One month after theoperation, histological observation indicated that in group A the regenerated nerves passed through the scaffold and in the new nerves there were regenerated blood vessels. The materials in groups B and C were not completely degraded. S-100 immunohistochemical observation and Bielschowsky staining showed that in groupB PDLLA-T3 repaired the defect successfully and the regenerated nerve myelinsheath was 1.81±0.19 μm in thickness. The effect in group B was better thanthat of groups A and C (P＞0.05). Two months after the operation, the materials in groups B and C were completely degraded. The quantity of the regeneratednerves in group B confirmed by S-100 immunohistochemical observation and Bielschowslcy staining was more than that in group C(P＜0.05) and close to that in group A. The regenerated nerve myelin sheath in group B was 2.15±0.27 μm in the thickness and was thicker than that in group C (P＜0.05)， but thinner than that in groups A and D (P＜0.05). Conclusion PDLLA-T3 can repair the defect of rat sciatic nerve with satisfactory quantity andquality of regenerated nerves.
OBJECTIVE To analysis the clinical characters of gluteal sciatic nerve injuries and investigate the treatment options. METHODS From October 1962 to June 1997, 190 patients with gluteal sciatic nerve injuries were adopted in this retrospective study. In these cases, the sciatic nerve injuries were caused by injection in 164 patients(86.32%), stab injury in 14 patients, pelvic fracture and hip dislocation in 11 patients, and contusion injury in 1 patient. Among them, 15 cases were treated by conservative method and the other 175 cases were operated. According to the observation during the operations, the injuries were occurred at the region of gluteal muscle in 146 cases, at the region of piriform muscle in 26 cases, and at the region of pelvic cavity in 3 cases. Then neurolysis was performed in 160 cases, epineurial neurorrhaphy in 12 cases and nerve grafting in 2 cases, and nerve exploration but no repair in 1 case. Late stage functional reconstruction of the foot and ankle was carried out in 23 cases. RESULTS One hundred and fifty-one patients were followed up 8.5 years in average. The occurrence of excellent and good nerve recovery was 56.95% and the occurrence of excellent and good functional reconstruction of late stage was 78.26%. CONCLUSION The gluteal sciatic nerve injury has since been challenging because of the tremendous difficulty in treatment and the poor outcome. The injury situation at the different region was closely related to the regional anatomy. According to this study, it is advised that the surgical treatment should be carried out actively. Neurolysis should be performed as soon as possible in the cases of injection injury. Epineurial neurorrhaphy should be performed in the cases of nerve rupture. In case of the gluteal sciatic nerve injury which caused by pelvic fracture or hip dislocation, the reduction and decompression is suggested in the early stage, and exploration and nerve repair is indicated in the late stage. The functional reconstruction of foot and ankle should be carried out in the late stage for the improvement of the limb function.
Objective To investigate whether the peri pheral administration of amitri ptyl ine and bupivacaine produces anti-hyperalgesic effect and to screen the neurotoxicological effect on sciatic nerve blockade in a rat model of neuropathic pain. Methods Twenty-four adult male SD rats [weighing (200 ± 20) g] were made the models of chronic constriction injury (CCI) and randomly divided into 3 groups (n=8) 5 days after operation: group A (amitriptyl ine), group B (bupivacaine) and group C (normal sal ine). 0.5 mL 0.5% amitriptyl ine, 0.5% bupivacaine or normal sal ine were given in group A, group B, and group C, respectively through implanted cannulas after 5, 7 and 9 days of CCI once a day for successive 3 days. The motor function was measured before administration and 1, 2, 4, 8, 12 and 24 hours after every administration. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured before administration and 1, 3, 5 and 7 days after the third administration. The operated sciatic nerve samples were obtained for neuropathological examination under l ight microscope. Results Twenty-four CCI rats were all survival without infection, palsy and catheter fall ing off. Compared with group C, the rats of group A and group B both produced significant ambulation deficits after every administration (P lt; 0.05). The ambulation deficits lasted 2 hours (group B) and 8 hours (group A) respectively. But the ambulation deficits of CCI rats were all reversible. The MWT and TWL of group A 1 and 3 days after the third administration increased when compared with those before administration and 5 and 7 days after the third administration, and when compared with group B and group C (P lt; 0.05). There was no significant difference (P gt; 0.05) in l ight microscopic neuropathological examination among three groups. Epineurial tissue and endoneurium tissue integrity, tidy arrangement of fibers, less inflammatory cell and no marked degeneration of myel inated fibers were observed. Conclusion Repeated sciatic nerve blockade with 0.5% amitriptyl ine has peripheral anti-hyperalgesic effects on neuropathic pain of rats. No morphological evidence of neurotoxicity in the sciatic nerve of rats is observed in 0.5% amitriptyl ine.
OBJECTIVE To probe the possibility of direct transfer of exogenous gene into peripheral nerve and its following expression in vivo. METHODS The PCMV beta plasmid containing cytomegalovirus (CMV) promoter and Escherichia Coli (E. Coli), beta-Galactosidease (beta-Gal) structural gene (lacZ gene) was constructed and injected into the rabbit sciatic nerve. The control group was injected PBS solution. The injected nerves were sampled and tested by beta-Gal enzyme activity assay of the 5-bromo-4-chloro-3-indolyl-beta-D-galactoside and beta-Gal histochemical stain. RESULTS In the control group, no beta-Gal enzyme activity was detected in the different stages after operation, and beta-Gal histochemical stains showed positive. In the experimental group, enzyme activity could be detected from 2 days to 30 days after operation, and the histochemical stains showed negative. CONCLUSION The exogenous gene can be transferred into peripheral nerve and expressed with bioactivity, thus the gene therapy to accelerate the recovery of nerve is practical.
Objective To explore a new method for the pre-degeneration of peripheral nerve in vitro for obtaining many effective Schwann cells so as to provide a large number of seed cells for the research and application of tissue engineered nerves. Methods The bone marrow derived cells (BMDCs) from transgenic green fluorescent protein C57BL/6 mouse and the sciatic nerve segments from the C57BL/6 mouse were co-cultured to prepare the pre-degeneration of sciatic nerve in vitro (experimental group, group A), and only sciatic nerve was cultured (control group, group B). At 7 days after culture, whether BMDCs can permeate into the sciatic nerve in vitro for pre-degeneration was observed by gross and immunohistofluorescence staining. And then Schwann cells were obtained from the sciatic nerves by enzymic digestion and cultured. The cell number was counted, and then the purity of primary Schwann cells was determined using immunohistofluorescence staining and flow cytometer analysis. Results At 7 days after pre-degeneration, gross observation showed that enlargement was observed at nerve stumps, and neuroma-like structure formed; the group A was more obvious than group B. Immunohistofluorescence staining showed many BMDCs permeated into the nerve segments, with positive F4/80 staining in group A. After culture, the yield of Schwann cells was (5.59 ± 0.19) × 104 /mg in group A and (3.20 ± 0.21) × 104/mg in group B, showing significant difference (t=2.14, P=0.03). At 48 hours after inoculation, the cells had blue bipolar or tripolar cell nuclei with small size and red soma by immunohistofluorescence staining; fibroblasts were flat polygonal with clear nucleus and nucleolus, showing negative p75NTR staining; and there were few of fibroblasts in group A. The purity of Schwann cells was 88.4% ± 5.8% in group A and 76.1% ± 3.7% in group B, showing significant difference (t=2.38, P=0.04). And the flow cytometer analysis showed that the purity was 89.6% in group A and 74.9% in group B. Conclusion BMDCs can promote the pre-degeneration of peripheral nerve in vitro, and it is a new method to effectively obtain Schwann cells for tissue engineered nerve.
Objective To investigate the time l imit of repairing old sciatic nerve defect in rats and observe the repair effect of autogenous nerve transplantation on old sciatic nerve defect in rats. Methods Thirty-six SD rats of clean grade wererandomized into 6 groups (n=6 per group). The animal model of nerve defect was made by transecting left sciatic nerve at the mid-thigh level. For groups A1, B1 and C1, defects were repaired by the contralateral autogenous nerve transplantation 1, 3 or 6 months after nerve damage and for the control groups of A2, B2 and C2, defects were not repaired. After operation, the gait, toe skin and leg muscle were examined weekly. Three months after autograft, a combination of electrophysiology examination, fluoro gold (FG) retrograde tracing and histological assessment including l ight microscopy, TEM was util ized to investigate the nerve functional recovery. Results Lameness and foot skin ulcers were observed in each group after nerve damage. At 2 months after autograft, such denervation symptoms were only improved in groups A1 and B1. At 3 months after autograft, the motor conduction velocity was (21.84 ± 6.74), (20.02 ± 4.17) and (16.09 ± 8.21) m/s in groups A1, B1 and C1, respectively, showing no statistically significant difference between them (P gt; 0.05). The ampl itude of compound muscle action potential (CAMP) was (12.68 ± 4.38), (9.20 ± 3.43) and (1.22 ± 0.39) mV in groups A1, B1 and C1, respectively, indicating significant differences between groups A1, B1 and group C1 (P lt; 0.05). No CAMP was evident in groups A2, B2 and C2. FG retrograde tracing conducted 3 months after autograft showed that the positive cells were most common in group A1 with big soma, mild in group B1 and lest in group C1 with smallest soma. Gastrocnemius Masson staining showed that the fiber morphology of gastrocnemius in groups A1 and B1 was close to normal, while the rest 4 groups had an obvious atrophy of muscle fiber. The fiber cross-section area was (340.73 ± 118.46), (299.88 ± 119.75), (54.33 ± 53.43), (78.60 ± 51.38), (65.62 ± 25.36), and (40.93 ± 28.22) μm2 in groups A1, B1, C1, A2, B2 and C2, respectively, indicating a significant difference between groups A1, B1 and groups C1, A2, B2 (P lt; 0.05). Neurohistology observation showed that more regenerated nerve fibers were observed in group A1 and B1, but less in group C1. The myel in sheath was thick in groups A1 and B1, while it was thin in group C1. Only SCs and hyperplastic collagen fiber were found in groups A2, B2 and C2. Conclusion Autogenous nerve transplantation is capable of repairing 1- and 3- month sciatic nerve defect to some degree in rat, but repair effect is not obvious on 6-month sciatic nerve defect in rats.