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Background PRF treatment has recently been described as minimally neurodestructive alternative to radiofrequency heat lesions. Patients with some pain syndromes in whom the pain could not be controlled by alternative techniques may be treated using PRF. In the present study, our main goal was to evaluate and compare the ultrastructure of peripheral nerve tissue that was heated by PRF, CRF with 42°C, and CRF with 70°C. Methods Forty-five male rats were divided into 5 groups. In PRF group and CRF with 42°C group, the sciatic nerve was heated at a temperature of 42°C for 120 seconds. As a positive control, some rat sciatic nerves were treated with CRF lesions at 70°C. The rats were kept alive for 21 days and then killed. Tissue was evaluated with transmission electron microscope, and grading was done to the groups. Results The unmyelinated nerve fibers were ultrastructurally normal in all groups. The results of myelinated axons indicated that PRF group had better grades, and CRF with 70°C group had the worst grade. Especially, comparison of the group of PRF and CRF with 42°C revealed significant difference. In PRF group, none of the myelinated axons showed severe degeneration findings, and most of the damaged myelinated axons showed only separation in myelin configuration. Conclusions PRF treatment may cause separation in myelinated axons. However, it seems that all changes were reversible. The present study supports the hypothesis that pulsed RF treatment does not rely on thermal injury of neurologic tissue to achieve its effect.

Background The neuroprotective effects of statins possibly depend on their pleiotropic effect such as antioxidative and anti-inflammatory properties. In this study, we have evaluated the efficiency of atorvastatin on brain edema, lipid peroxidation, and ultrastructural changes in TBI animal model. Methods Modified Feeney method has been used for the trauma model in rats. Only craniectomy for group A and trauma after craniectomy for group B was the procedure for animals. For the trauma, rods weighing 24 g were dropped on a foot plate just over the dura. Atorvastatin (1 mg/kg, IP) was administered to the animals in group C after craniectomy and trauma; but on the other hand, animals in group D received only 0.5 mL PEG as the vehicle. Brains were harvested 24 hours after the trauma for the assays of wet-dry weight, lipid peroxidation level, and ultrastructural investigations. Lipid peroxidation levels, TEM, and UNGS were the investigated parameters. The statistical comparisons between the groups were investigated by 1-way ANOVA and post hoc analysis by Duncan and Dunnett T3 test within the groups at the significance level P = .05. Results Trauma increased water contents of the brain tissues and lipid peroxidation levels in groups B and D. When compared with the results of group B (brain edema, 84.694% ± 1.510%; lipid peroxidation, 74.932 ± 2.491 nmol/g tissue), atorvastatin (1 mg/kg) significantly decreased brain edema (77.362% ± 1.448%), lipid peroxidation level (58.335 ± 3.980 nmol/g tissue), and UNGS scores in group C ( P Conclusion In this descriptive study, the remarkable improvements of atorvastatin on brain edema, lipid peroxidation, and ultrastructural investigations encouraged us for a further dose optimization study.

The purpose of this study was to investigate the effect of EPO on LPO, on ultrastructural findings, and on antiapoptotic bcl-2 and survivin gene expressions after TBI. The authors also compared the activity of EPO with that of MPSS.Wistar rats were divided into 6 groups: sham-operated, control, moderate TBI-alone (300 g/cm), TBI + EPO-treated (1000 IU/kg), TBI + MPSS-treated (30 mg/kg), and TBI + vehicle-treated (0.4 mL albumin solution) groups.Compared with the levels in control and sham-operated animals, LPO was significantly elevated in rats in the trauma-alone group. The administration of EPO and MPSS significantly decreased the LPO levels (P.05). Trauma also increases the antiapoptotic bcl-2 gene expression significantly at 24 hours postinjury (P.05), but it has no effect on survivin expression. The EPO and MPSS treatments caused significant elevation in both gene expressions (P.05). It is also showed that MPSS has more protective effect than EPO on brain ultrastructure, especially on the structure of small- (P.05) and medium-sized myelinated axons, after TBI.EPO has protective effects after moderate TBI, and this effect seems better than MPSS on antiapoptotic gene expression and LPO. The protection of cerebral subcellular organelles after traumatic injury is more prominent in MPSS-treated animals than EPO-treated animals quantitatively. This experimental study indicates that the benefits of EPO in the management of TBI have promising results and prompts further studies on the difference between EPO and MPSS in histopathological findings at the subcellular level.

Background Spinal cord injury (SCI) is a common and often irreversible lesion that can incapacitate patients. Precursor cells in the spinal cord proliferate in response to trauma, and this proliferation can be enhanced by exogenous stimuli such as specific growth factors. In the present study, we examined electron microscopic detection of the proliferation, distribution, and phenotypic fate of these precursor cells in the injured adult rat spinal cord. Methods Adult female Sprague-Dawley rats weighing 250 to 300 g were divided into 3 groups. The first group consisted of spinal cord–injured animals with application of a 2.4-g clip extradurally around the spinal cord at the T1 level. A 26-g clip was applied in the second group. The third group included normal uninjured animals. Rats were sacrificed at 3 days, 3 weeks, and 6 weeks after injury. A segment of the spinal cord, 0.4 cm in length, encompassing the injury site was removed and was prepared for electron microscopy. Results Three days after mild injury (2.4-g clip), ependymal cells had begun to proliferate and had migrated from the central canal. They had a tendency to surround perivascular spaces close to the axons. The central canal rostral to the lesion site was widely dilated at 6 weeks postoperative in the moderately injured groups (26-g clip). The layer of ependymal cells lining the dilated canal showed reduction in cell height. Traumatic syringomyelic cavities were observed in all of the animals. There was an active proliferative response of the ependymal cells to injury. Large clusters of displaced ependymal cells associated with the dilated central canal were observed. Rests of ependymal cells were observed remote from the central canal with a tendency to form rosettes and accessory lumina 6 weeks after trauma. Fascicles of 3 to 8 fibers enclosed within an ependymal cell were a common finding among the ependymal clusters. There were also debris and some ependymal cells in the lumen. Conclusion Trauma induces active proliferation of precursor cells in the ependymal region. These cells may replace neural tissue lost to SCI and may assist in axonal regeneration.

The aims of this study were to evaluate the efficiency of dexamethasone sodium phosphate (DSP) in the treatment of cold injury-induced brain edema and to compare systemic and topical application of DSP.Sprague-Dawley rats weighing nearly 300 g were used in the experiments. Brain edema was formed by cold injury using metal sterile rods with a diameter of 4 mm that were previously cooled at -80 degrees C. Twenty-four hours after the injury, animals were decapitated and brain tissues were investigated by wet-dry weight method, lipid peroxidation ratio, and histological examination.The degree of edema was significantly lowered in groups in which DSP was administered using chitosan microspheres and by intraperitoneal route (P.05). The statistical evaluation of the experimental results was performed using Mann-Whitney U test. Histological findings transmission electron microscopy (TEM) correlated with the quantitative results.Both intraperitoneal- and microsphere-administered DSP were found to be very effective in a cold injury brain edema model. The authors believe that future studies should lead to new applications of the microsphere formulations prepared by chitosan as the matrix material in many other therapies.