Intratympanic Insulin-like Growth Factor-1 Administration Via the Otic Bulla in a Severe Facial Paralysis Model.

HYPOTHESIS: We investigated the treatment effect of intratympanic insulin-like growth factor-1 (IGF-1) on severe facial paralysis in guinea pigs. BACKGROUND: The use of regenerative medicine involving growth factors has been reported in the treatment of peripheral nerve diseases. IGF-1 plays a crucial role in nerve regeneration. METHODS: We performed the following procedures on guinea pigs. In the normal group (n = 7), no procedure was performed. In the saline (n = 7) and IGF-1 (n = 7) groups, facial paralysis was induced by freezing of the facial canal. Subsequently, in the saline and IGF-1 groups, a gelatin hydrogel impregnated with 100 µL saline and 400 µg/100 µL IGF-1, respectively, was placed in the facial canal. Facial nerve functions were evaluated using three test batteries: facial movement observation, electrophysiological testing, and histological assessment. RESULTS: At 10 weeks postoperatively, the facial movement scores for the IGF-1 group were improved compared to those in the saline group. The conductive velocity was significantly faster in the IGF-1 group than in the saline group. There was a significant between-group difference in the nerve fiber number and myelin thickness. CONCLUSION: Intratympanic IGF-1 administration improved facial nerve regeneration. This novel method could provide prompt ambulatory regenerative treatment and reduce the incidence of poor recovery in patients with severe facial paralysis.

Non-recovery animal model of severe facial paralysis induced by freezing the facial canal.

OBJECTIVE: Some cases of peripheral facial paralysis are resistant to treatment, thus, a non-recovery model of facial paralysis is needed to develop new treatment strategies for this condition. The purpose of the current study was to develop an animal model of which facial palsy was severe and prolonged. METHODS: Ten 8-week-old female Hartley guinea pigs weighing between 400 and 500 g were used for the animal model. The vertical segment of the facial canal was accessed via the otic bulla, without removing the bony wall of the facial canal. The canal was then frozen for 5 s using freeze spray. Facial movements, electroneurography (ENoG), histology, and changes in temperature were evaluated. RESULTS: All animals exhibited complete facial paralysis immediately after the procedure and recovered gradually, however, not all of them had recovered completely 15 weeks after freezing. The ENoG values one week after freezing for all animals (10/10) were 0%. Histological examination one week after freezing revealed that most of the vertically placed myelinated nerve fibers which had been frozen were remarkably affected and denatured. The number of vertically placed myelinated nerve fibers increased 15 weeks after freezing, but the nerve fibers were smaller than normal nerve fibers and were distorted in shape. CONCLUSION: Complete facial paralysis was induced in Hartley guinea pigs by freezing the facial canal. The behavioral, ENoG, and histopathological data suggest that the facial paralysis was severe and prolonged. This model may assist in developing novel treatment for severe facial palsy and facilitate basic research on facial nerve regeneration.