The effects of lipoic acid and methylprednisolone on nerve healing in rats with facial paralysis.

OBJECTIVE: To investigate the effects of lipoic acid and methylprednisolone on nerve healing in rats with traumatic facial paralysis. MATERIALS AND METHODS: The rats were randomly divided into four groups, with six rats in the control group and eight each in the remaining three groups. The buccal branch of the facial nerve in all groups except the control group was traumatized by a vascular clamp for 40 minutes. Group 1 was given lipoic acid (LA), Group 2 was given methylprednisolone (MP), and Group 3 was given lipoic acid and methylprednisolone (LA + MP) for one week. Nerve stimulus thresholds were measured before trauma, after trauma and at the end of the one week treatment period. RESULTS: When the groups were compared with each other, post-treatment threshold levels of LA + MP were significantly lower than LA. Although post-treatment threshold levels of LA and MP were still higher than the control group, there was no significant difference between LA + MP and control values (p > .05). CONCLUSION: Lipoic acid has a positive effect on nerve healing and can enhance the effect of methylprednisolone treatment. It is a good alternative in cases where methylprednisolone cannot be used.

Effects of ozone therapy on facial nerve regeneration / Efeitos da terapia com ozônio na regeneração do nervo facial

Abstract Introduction: Ozone may promote moderate oxidative stress, which increases antioxidant endogenous systems. There are a number of antioxidants that have been investigated therapeutically for improving peripheral nerve regeneration. However, no previous studies have reported the effect of ozone therapy on facial nerve regeneration. Objective: We aimed to evaluate the effect of ozone therapy on facial nerve regeneration. Methods: Fourteen Wistar albino rats were randomly divided into two groups with experimental nerve crush injuries: a control group, which received saline treatment post-crush, and an experimental group, which received ozone treatment. All animals underwent surgery in which the left facial nerve was exposed and crushed. Treatment with saline or ozone began on the day of the nerve crush. Left facial nerve stimulation thresholds were measured before crush, immediately after crush, and after 30 days. After measuring nerve stimulation thresholds at 30 days post-injury, the crushed facial nerve was excised. All specimens were studied using light and electron microscopy. Results: Post-crushing, the ozone-treated group had lower stimulation thresholds than the saline group. Although this did not achieve statistical significance, it is indicative of greater functional improvement in the ozone group. Significant differences were found in vascular congestion, macrovacuolization, and myelin thickness between the ozone and control groups. Significant differences were also found in axonal degeneration and myelin ultrastructure between the two groups. Conclusion: We found that ozone therapy exerted beneficial effect on the regeneration of crushed facial nerves in rats.

Resumo Introdução: O ozônio pode promover estresse oxidativo moderado, o que aumenta sistemas endógenos antioxidantes. Há determinado número de antioxidantes sendo investigados terapeuticamente para melhorar a regeneração do nervo periférico. No entanto, nenhum estudo anterior relatou o efeito da terapia com ozônio na regeneração do nervo facial. Objetivo: Nosso objetivo foi avaliar o efeito da terapia com ozônio na regeneração do nervo facial. Método: Ao todo, 14 ratos albinos Wistar foram divididos aleatoriamente em dois grupos com lesões experimentais por esmagamento do nervo: um grupo controle, que recebeu tratamento com solução salina pós-esmagamento; e um grupo experimental, que recebeu tratamento com ozônio. Todos os animais foram submetidos a cirurgia na qual o nervo facial esquerdo foi exposto e esmagado. O tratamento com solução salina ou ozônio se iniciou no dia do esmagamento do nervo. Os limiares de estimulação do nervo facial esquerdo foram medidos antes do esmagamento, imediatamente após o esmagamento e após 30 dias. Depois de medir limiares de estimulação do nervo aos 30 dias pós-lesão, o nervo facial esmagado foi excisado. Todas as amostras foram estudadas por meio de microscopia óptica e eletrônica. Resultados: Após o esmagamento, o grupo tratado com ozônio apresentou menores limiares de estimulação do que o grupo da solução salina. Embora isso não tenha significância estatística, é indicativo de maior melhoria funcional no grupo do ozônio. Foram encontradas diferenças significativas na congestão vascular, macrovacuolização e espessura da mielina entre os grupos do ozônio e controle. Diferenças significativas também foram encontradas na degeneração axonal e ultraestrutura de mielina entre os dois grupos. Conclusão: Verificou-se que a terapia com ozônio teve efeito benéfico sobre a regeneração dos nervos faciais esmagados em ratos.

Effects of ozone therapy on facial nerve regeneration.

INTRODUCTION: Ozone may promote moderate oxidative stress, which increases antioxidant endogenous systems. There are a number of antioxidants that have been investigated therapeutically for improving peripheral nerve regeneration. However, no previous studies have reported the effect of ozone therapy on facial nerve regeneration. OBJECTIVE: We aimed to evaluate the effect of ozone therapy on facial nerve regeneration. METHODS: Fourteen Wistar albino rats were randomly divided into two groups with experimental nerve crush injuries: a control group, which received saline treatment post-crush, and an experimental group, which received ozone treatment. All animals underwent surgery in which the left facial nerve was exposed and crushed. Treatment with saline or ozone began on the day of the nerve crush. Left facial nerve stimulation thresholds were measured before crush, immediately after crush, and after 30 days. After measuring nerve stimulation thresholds at 30 days post-injury, the crushed facial nerve was excised. All specimens were studied using light and electron microscopy. RESULTS: Post-crushing, the ozone-treated group had lower stimulation thresholds than the saline group. Although this did not achieve statistical significance, it is indicative of greater functional improvement in the ozone group. Significant differences were found in vascular congestion, macrovacuolization, and myelin thickness between the ozone and control groups. Significant differences were also found in axonal degeneration and myelin ultrastructure between the two groups. CONCLUSION: We found that ozone therapy exerted beneficial effect on the regeneration of crushed facial nerves in rats.

Nimodipine-mediated re-myelination after facial nerve crush injury in rats.

This study aimed to investigate the mechanism of nimodipine-mediated neural repair after facial nerve crush injury in rats. Adult Sprague-Dawley rats were divided into three groups: healthy controls, surgery alone, and surgery plus nimodipine. A facial nerve crush injury model was constructed. Immediately after surgery, the rats in the surgery plus nimodipine group were administered nimodipine, 6 mg/kg/day, for a variable numbers of days. The animals underwent electromyography (EMG) before surgery and at 3, 10, or 20 days after surgery. After sacrifice, nerve samples were stained with hematoxylin and eosin (H&E) and luxol fast blue. The EMG at 20 days revealed an apparent recovery of eletroconductivity, with the surgery plus nimodipine group having a higher amplitude and shorter latency time than the surgery only group. H&E staining showed that at 20 days, the rats treated with nimodipine had an obvious recovery of myelination and reduction in the number of infiltrating cells, suggesting less inflammation, compared with the rats in the surgery only group. Luxol fast blue staining was relatively even in the surgery plus nimodipine group, indicating a protective effect against injury-induced demyelination. Staining for S100 calcium-binding protein B (S-100ß) was not evident in the surgery alone group, but was evident in the surgery plus nimodipine group, indicating that nimodipine reversed the damage of the crush injury. After a facial nerve crush injury, treatment with nimodipine for 20 days reduced the nerve injury by mediating remyelination by Schwann cells. The protective effect of nimodipine may include a reduction of inflammation and an increase in calcium-binding S-100ß protein.

Vitamin D3 potentiates myelination and recovery after facial nerve injury.

Roles of vitamin D on the immune and nervous systems are increasingly recognized. Two previous studies demonstrated that ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) induced functional recovery and increased myelination in a rat model of peroneal nerve transection. The current report assessed whether cholecalciferol was efficient in repairing transected rabbit facial nerves. Animals were randomized into two groups of rabbits with an unilateral facial nerve surgery: the vitamin D group included animals receiving a weekly oral bolus of vitamin D3 (200 IU/kg/day), from day 1 post-surgery; the control group included animals receiving a weekly oral bolus of vehicle (triglycerides). Contralateral unsectioned facial nerves from all experimental animals were used as controls for the histological study. The facial functional index was measured every week while the inner diameter of myelin sheath and the G ratio were quantified at the end of the 3 month experiment. The current report indicates that cholecalciferol significantly increases functional recovery and myelination, after 12 weeks of treatment. To the best of our knowledge, this is the first study investigating the therapeutic benefit of vitamin D supplementation in an animal model of facial paralysis. It paves further the way for clinical trials based on the administration of this steroid in individuals with injured facial nerves.

Effect of ginkgo biloba extract on recovery after facial nerve crush injury in the rat.

BACKGROUND AND OBJECTIVE: Many pharmacological agents have shown successful results in experimental crush injury of the peripheral nerve. To date, therapeutic effect of ginkgo biloba extract (GBE) on the peripheral nerve crush injury of rats has been rarely reported, moreover, neuroprotective effect on the facial nerve crush injury has not been reported. MATERIALS AND METHODS: Prospective functional recovery, using a vibrissae movement and electrophysiological analysis of recovery 4 weeks after the facial nerve crush in adult rats, and comparison with randomized intraperitoneal injection of either GBE or control phosphate buffered saline. RESULTS: Relative to the control group (26 days post operation), administration of GBE significantly accelerated the recovery of vibrissae orientation to 11.7 days post the operation. A significant functional recovery was observed by postoperative 2nd week in the experimental group. The recovery of threshold and conduction velocity, postoperative 4th week in the experimental group, showed statistically significant difference compared to that of the control group. CONCLUSION: From this result, intraperitoneal injection of GBE has been found effective in promoting the regeneration of the nerve in an experimental facial nerve crush rat model. Further studies, including morphological and molecular analyses, are necessary to clarify the mechanisms of GBE on the facial nerve crush.

Nimodipine promotes regeneration of peripheral facial nerve function after traumatic injury following maxillofacial surgery: an off label pilot-study.

BACKGROUND: Animal tests, retro- and prospective clinical trials in neurosurgical departments have shown a beneficial effect of nimodipine on the preservation and recovery of facial and acoustic nerve function following vestibular schwannoma surgery. Encouraged by these positive results a pilot-study of nimodipine treatment in patients with a peripheral facial nerve (FN) paresis following maxillofacial surgery was performed. The rate and time of FN recovery were analysed and compared with the results in the literature. METHODS: Thirteen patients (n = 13) suffering from a moderate (1/13) up to a severe (12/13) peripheral FN paresis after maxillofacial surgery were treated with orally administered nimodipine. The anatomical main course of the FN was preserved in all patients with a 2nd to 3rd degree of Sunderland-injury (Sunderland, 1951). After no evidence of a spontaneous regeneration had shown, oral medication with nimodipine was started as an "off-label" use. RESULTS: An improvement of the FN function correlated to the start of the vasoactive medication and as a consequence a recovery of the FN function up to House-Brackmann (HB) grade I°-II° was observed in all the patients within a period of 2 months after the beginning of treatment (p = 0.00027). CONCLUSIONS: The clinical observations in these patients suggest a positive effect of nimodipine on the acceleration of peripheral FN regeneration after surgically caused trauma. The results of this pilot-study are very promising. A prospective study with a larger number of patients is planned to approve the beneficial effect of nimodipine on the peripheral FN in maxillofacial or otorhinolaryngological surgery.