Changes following the injury to sciatic nerve caused by high intensity ultrasound in rabbits

Objective To determine the changes in action potential peak value and maximal nerve conduction velocity of rabbit sciatic nerve after being exposed to different doses of high intensity ultrasound (HIU) and establish the experimental basis for the use of HIU in patients with refractory pain. Methods Eighty New Zealand white rabbits of either sex weighing 2.0-2.5 kg, aged 5-10 months were randomly divided into four groups with 20 rabbits in each group :group Ⅰ 0 second;group Ⅱ 15 seconds;group Ⅲ 25 seconds and group Ⅳ 50 seconds. The animals were anesthetized and placed in the prone position. Sciatic nerves were exposed to 4 different doses of HIU (7.1 MHz, 40 W/cm2 f55 0 s, 15 s, 25 s, 50 s) in the four groups. The animals were allowed to recover. At 5 intervals (1 and 2 weeks, 1, 3 and 6 months) after exposure to HIU, 4 animals in each group were anesthetized and recording electrodes were placed on sciatic nerves at 2 cm distal to the site of HIU radiation, tibial and sural cutaneous nerves. The amplitude (peak value) and latency of action potential and maximal conduction velocity of the nerves were recorded. Sciatic nerves were obtained from one of the four animals for light and electron microscopic examination. Results The larger was the dose of HIU, the more time was needed for the injuried nerve to recover. In group Ⅰ (0 s) there were no significant changes in action potential peak value and maximal nerve conduction velocity at any interval after exposure to HIU;in group Ⅱ (15 s) there were slight changes in the electrophysiological parameters and the changes recorded on tibial nerve returned to normal soon while those recorded on sural cutaneous nerve returned to normal one month later; in group Ⅲ (25 s) there were significant changes in the electrophysiological parameters and it took 3 months for tibial nerve but 6 months for sural cutaneous nerve to recover;in group Ⅳ (50s) the nerves were completely blocked, no action potential was recorded and no recovery was observed after 6 months. Light and electron microscopic examination showed that in group 1 no significant changes of nerves were observed; in group Ⅱ there was slight deformation of myelin sheath which returned to normal 2 weeks later; in group Ⅲ sheath was broken or lost, and axon degeneration was observed at 1 week after exposure to HIU and the changes disappeared 1 month later; in group Ⅳ necrosis of the nerve was observed and no recovery was observed 6 months later. Conclusion HIU can be used for the treatment of refractory pain. Analgesia can be achieved with loss of only part of motor function. The nerve can be permanently blocked by HIU if necessary.