ABSTRACT
BACKGROUND: Recent studies in invertebrates have taught us that early cell membrane regeneration is determinant for axonal recovery and survival after trauma. Many authors obtained extraordinary results in neural regeneration using polyethylene glycol fusion protocols, which also involved microsutures and antioxidants. METHODS: Sixty rats were evaluated with functional and histological protocol after facial nerve neurotmesis. Groups A and B had their stumps coapted with microsuture after 24 hours of neurotmesis and groups C and D after 72 hours. In addition to the microstructure, groups B and D used the polyethylene glycol-fusion protocol for the modulation of the Ca+2 . RESULTS: At the sixth week, the latency of group D and duration of group B was lower than groups A and C (P = .011). The axonal diameter of the groups that used polyethylene glycol-fusion was higher than those who did not use polyethylene glycol-fusion (P ≤ .001). CONCLUSION: Although not providing a functional improvement, polyethylene glycol-fusion slowed down demyelination.
Subject(s)
Facial Nerve Injuries/drug therapy , Facial Paralysis/drug therapy , Polyethylene Glycols/pharmacology , Action Potentials , Animals , Axons/pathology , Calcium/pharmacology , Facial Nerve Injuries/surgery , Facial Paralysis/etiology , Models, Animal , Nerve Regeneration/drug effects , Rats, WistarABSTRACT
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.
Subject(s)
Animals , Rats , Ozone/therapeutic use , Facial Nerve Injuries/drug therapy , Nerve Regeneration/drug effects , Ozone/administration & dosage , Rats, Wistar , Facial Nerve Injuries/pathology , Disease Models, AnimalABSTRACT
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.
Subject(s)
Facial Nerve Injuries/drug therapy , Nerve Regeneration/drug effects , Ozone/therapeutic use , Animals , Disease Models, Animal , Facial Nerve Injuries/pathology , Ozone/administration & dosage , Rats , Rats, WistarABSTRACT
OBJECTIVE: To analyze the influence of the topical use of basic fibroblast growth factor (bFGF) in the regeneration of the facial nerve in rats. STUDY DESIGN: Experimental study. MATERIALS AND METHODS: Twenty-eight Wistar adult male rats underwent complete section of the facial nerve trunk, followed by end-to-end anastomosis with epineural sutures. An osmotic minipump equipped with a delivery catheter was implanted subcutaneously near the neural anastomosis. During the subsequent 14 days, 14 animals received a solution containing 25 microg/ml of bFGF, 250 UI/ml of sodium heparin, and 1,000 microg/ml of human albumin diluted in Ringer lactate, and 14 animals received a control solution of the same components without bFGF. To evaluate facial nerve regeneration, the number of myelinated fibers evident on histologic sections was counted on the 14th (7 experimental and 8 control animals) and the 28th days (7 experimental and 6 control animals) after surgery, and the facial movements of vibrissae and the blink reflex were evaluated on alternate days until the 28th day. RESULTS: On histologic evaluation, the number of myelinated fibers was similar between groups on the 14th day and greater in the group that received bFGF on the 28th day. Behavioral evaluation showed that the animals of the bFGF group presented better functional results between the 6th and 16th days for the blink test and the 14th to the 16th days for vibrissae movements. CONCLUSION: This study showed that the regeneration of the facial nerve occurred earlier and resulted in significantly more myelinated nerve fibers in the animals that received topical bFGF.
Subject(s)
Facial Nerve Injuries/drug therapy , Fibroblast Growth Factor 2/administration & dosage , Nerve Fibers, Myelinated/drug effects , Nerve Regeneration/drug effects , Recovery of Function/drug effects , Administration, Cutaneous , Animals , Blinking/drug effects , Cell Count , Facial Nerve Injuries/pathology , Facial Nerve Injuries/physiopathology , Male , Nerve Fibers, Myelinated/pathology , Rats , Rats, Wistar , Statistics, Nonparametric , Vibrissae/drug effectsABSTRACT
CONCLUSIONS: Riluzole promoted increase and/or preservation of axon density in the animals treated with this drug as compared to the control group; it did not increase the mean diameter of facial nerve fibres as compared to the non-treated group; and it did not provide a better functional motor recovery than in the control group. OBJECTIVE: Traumatic peripheral facial paralysis is a frequent affection. In incomplete nerve injuries, systemic drugs acting on regeneration may decrease the patient's period of morbidity. This study aimed to determine the effect of the drug riluzole on regeneration of the facial nerve of rabbits submitted to post-traumatic facial paralysis. MATERIALS AND METHODS: Eighteen rabbits were submitted to compression of the facial nerve and divided into control (A) and treated (B) groups. The animals were sacrificed 4 weeks after the injury and their nerves were studied regarding density of myelinated axons and measure of external axon diameters. RESULTS: Partial functional recovery was observed within 2 weeks and complete recovery 5 weeks after injury. Mean neural density was 12,679.7 axons/mm2 (SD+/-237.5) in group A, and 19,073.8 axons/mm2 (SD+/-3549.9) in group B. Group A presented less than two-thirds the density of group B. There was no statistical difference in axon diameters between the studied groups.