MATERIALS AND METHODS: Five groups composed of 5 rats each were used in the study.

Group 1: The control group, in which a 1 cm-long segment proximally from the bifurcation point of the right sciatic nerve of each rat was excised, accompanied by removal of the right soleus muscle. Group 2: The compression neuropathy model group, in which the right sciatic nerve of each rat was compressed for 30 days. Group 3: The right sciatic nerves were compressed for 30 days, followed by decompression and assessment on the 60th day. Group 4: The right sciatic nerves were compressed for 30 days, followed by decompression and acetyl-Lcarnithine administration between days 30 and 60. Group 5: The right sciatic nerves were compressed for 30 days, followed by acetyl-L-carnithine administration from day 30 to 60 without decompression. The study continued with the rats in the other 3 groups. Rats in the 3rd group were treated with decompression only and kept for another 1 month. Rats in the 4th group received acetyl-L-carnithine at a dose of 20 mg/kg/day intraperitoneally for 1 month after decompression, whereas rats in the 5th group received only intraperitoneal acetyl-L-carnithine at a dose of 20 mg/kg/day without decompression. Like the rats in groups 1 and 2, these rats were also sacrificed with ether overdose, with their right sciatic nerves and soleus muscles being excised for histopathological examination and weighing, respectively.

CONCLUSION: In our study, it was found that decompression significantly improves the recovery rate of peripheral nerve as compared with that without d e c o m p ression, and that acetyl-L-carnithine coadministered with decompression enhances clinical and histopathological recovery. In addition, the use of silicon tubes in such experiments was found to be likely to have prominent advantages. Keywords : Acetyl-L-carnithine, Ch ronic nerve compression , Neuroprotective effects