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J Korean Acad Rehabil Med. 1998 Aug;22(4):908-920. Korean. Original Article.
Lee MH , Kwon HK , Kim HK .
Department of Rehabilitation Medicine, Sam Yook Rehabilitation Hospital.
Department of Rehabilitation Medicine, College of Medicine, Korea University.
Department of Pathology, College of Medicine, Korea University.
Abstract

OBJECTIVE: To investigate the electrophysiologic and histopathologic changes of the prheral nerve from hyperthermal nerve injury and to observe the difference of these changes according to the level of temperature and the duration of heat application. METHOD: The experimental rats (Sprague-Dawley) were divided into four groups according to the degree of temperature and the duration of heat application : Group 1, 43degrees C for 15 min; Group 2, 43degrees C for 30 min; Group 3, 45degrees C for 15 min; Group 4, 45degrees C for 30 min. A segment of 5 mm of the sciatic nerve was exposed and treated in vivo with local hyperthermia using a thermostatically controlled heating unit. For the electrophysiologic examination, both sciatic nerve conduction study and needle electromyographic examination were performed immediately before, and at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hyperthermia. For the histopathologic study, a sciatic nerve biopsy was performed at 1 day, 1 week, 2 weeks, and 4 weeks after the hyperthermia and the changes were investigated under the light microscopic and electronmicroscopic examinations. RESULTS: In experimental groups, the compound muscle action potentials (CMAPs) showed a significant reduction compared to the control group (p<0.05). Amplitudes of CMAPs following the heat application to the nerve were inversely related with the degree and duration of hyperthermia. A significant recovery of CMAPs was observed at 4 weeks after the hyperthermia in all experimental groups. The motor conduction latencies, however, did not show any significant changes. The needle electromyography of the gastrocnemius began to reveal fibrillation potentials on the 3rd day after the hyperthermia and continued to appear until the second week and then completely disappeared at 4 weeks after the hyperthermia. The histopathologic findings began to show the degeneration of axon and myelin within 24 hours and a remarkable regeneration at 4 weeks after the hyperthermia. CONCLUSION: The results revealed that the hyperthermia of peripheral nerve within the range of 43~45degrees C for 15~30 min is likely to cause a significant acute, but not necessarily permanent nerve injury, and the severity of nerve injuries is related to the temperature and duration of heat applications. Whether the results can be clinically applied to human beings would require further exploration.

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