• The Korean Journal of Pain
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• v.13 no.2
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• pp.149-155
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• 2000

Background: Pulsed radiofrequency (RF) lesioning is a painless procedure and causes no neurodestruction and neuritis-like reaction are common following conventional RF lesioning. There is little data about the effect of pulsed RF especially with regard to its suitability for the treatment of acute pain. The possibility of a placebo effect cannot be ruled out because a double-blind study was not performed in previous studies. There is also no neuropathologic study about pulsed RF. Methods: The rats were anesthetized with sodium pentobarbital (40 mg/kg, i.p.; supplemented as necessary). The common sciatic nerve was exposed by blunt dissection through biceps femoris. Pulsed RF was administered to the common sciatic nerve using a 30 ms/s pulse with for 120 seconds. The temperature reached was no more than $42^{\circ}C$. Analgesia was determined using hot-plate assay shortly and, 3 days and 1 week before, and 2 weeks after operation. Lesions were examined with LM (light microscope) and EM (electron microscope) 2 weeks later. Results: There were no differences in response latencies between the control and experimental group. There were many vacuoles with hyaline bodies in the Schwann cell cytoplasm rather than axon in LM and larger electron dense bodies. No changes were found in the axon or unmyelinated fibers. Only small changes were found in the sheaths of myelinated fibers and Schwann cells. Conclusions: We therefore do think that any analgesic effect of pulsed RF is not a result of block of neural conduction. But rather than it can be attributed to others factors. It was also ineffective as a treatment for acute pain such as that caused by the hot-plate test.

• Progress in Medical Physics
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• v.14 no.4
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• pp.259-267
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• 2003

In vivo $^1$H magnetic resonance spectroscopy (MRS) at 4.7 T was applied to investigate the cerebral metabolite changes of mice brain before and after experimental brain trauma. In vivo $^1$H MR spectra were acquired from a voxel covering right parietal cortex in normal brain, used as control subjects. After experimental brain trauma using the fluid percussion injury (FPI) method, $^1$H MR spectra were acquired from the same lesion three days after trauma. Metabolite ratios of the injured lesion were compared to those of controls. After trauma, N-acetylaspartate (NAA)/creatine (Cr) ratio, as a neuronal marker was decreased significantly versus controls, indicating neuronal loss. The ratio of NAA/Cr in traumatic brain contusion was 0.90$\pm$0.11, while that in normal control subjects was 1.13$\pm$0.12 (P=0.001). Choline (Cho)/Cr ratio had a tendency to rise in experimental brain contusion (P=0.02). Cho/Cr ratio after trauma was 0.91$\pm$0.17 while that before traumas was 0.76$\pm$0.15. Cho/Cr ratio was increased and this might indicate a inflammatory activity. However, no significant difference of [(glutamate＋glutamine) (Glx)]/Cr was established between experimental traumatic brain injury models and normal controls. Lactate (Lac)/Cr ratio was appeared as a sign of shifted posttraumatic energy metabolism and increased versus controls. These findings strongly suggest that in vivo $^1$H MRS may be a useful modality for clinical evaluation of traumatic contusion and could aid in better understanding the neuropathologic process of traumatic contusion induced by FPI. In the present study, in vivo $^1$H MRS was proved to be a useful non-invasive method for in vivo diagnosis and monitoring of posttraumatic metabolism in models of brain contusion.