Electrophysiological and histopathological evaluation of the effects of glatiramer acetate and melatonin's systemic and local uses in traumatic faceal injury

Objective: Traumatic facial nerve injury is frequently seen in daily life and can cause functional, cosmetic and psychological problems in individuals. The treatment of facial nerve injuries has an important place in the clinic, and new studies are added to the literature every day to improve treatment options in addition to the surgical and medical treatments used today. In this study, we aimed to evaluate the effects of melatonin and glatiramer acetate on nerve regeneration in traumatic nerve injury models electrophysiologically and histopathologically. Materials and Methods: In our study, 42 Wistar Albino male rats were used. The subjects were randomly divided into 6 equal groups as healthy control, damaged control, systemic melatonin, local melatonin, systemic glatiramer acetate and local glatiramer acetate. Except for the healthy control group, the right facial nerve trunks of all subjects were damaged with the "crush injury" model. After the relevant treatment procedure was applied to each group, the rats were followed for 4 weeks. The motor functions of the facial nerve were recorded electrophysiologically in all rats in the study groups before and at the end of the surgery, and the damaged nerve area was resected and evaluated histopathologically. Results: In the electrophysiological examination, when compared with the pre-injury and post-injury data of all treatment groups and the control group, it was shown that the control group was the group with the greatest decrease in amplitude value and the most prolonged latency value. Only in the systemic melatonin group, both the decrease in amplitude and the increase in latency were found to be significantly positive compared to the control group. In the comparison between the treatment groups according to amplitude and latency, a treatment group in which both evaluations showed a positive correlation could not be determined. In the histopathological evaluation, both axon surface area and histological damage scoring were significantly positive in all treatment groups compared to the damage control group. Conclusion: It has been shown both histologically and electrophysiologically that melatonin and glatiramer acetate have a positive effect on regeneration in traumatic facial nerve injury. Both agents are thought to be an effective treatment for peripheral nerve regeneration. More comprehensive studies are needed to determine the appropriate dose and duration of treatment. Keywords: facial nerve, peripheral nerve regeneration, melatonin, glatiramer acetate