Abstract
Background: The incidence of incomplete facial paralysis is now relatively higher in clinical practice, and surgical intervention is still desirable for patients with significant facial paralysis. However, the importance and usefulness of the remaining and/or spontaneously regenerated facial axons for regaining facial function when using hypoglossal–facial nerve (HN-FN) neurorrhaphy or other nerve-transferring methods to treat facial paralysis remain controversial.Objective: We designed a rat FN injury model with preservation of the anatomical structure followed by HN-FN side-to-side neurorrhaphy to investigate the effects of the remaining and/or spontaneously regenerated FN axons on restoration of facial function.Methods: After the evident return of facial function in 3 months following FN injury and HN-FN side-to-side neurorrhaphy, the FN was cross-sectioned again according to different ratios (0, 30, 70, and 100%) at the site rostral to the initial FN injury to retain, partially abolish, or completely abolish the spontaneously regenerated FN axons that had successfully reinnervated the paralyzed facial muscles. Then, FN function was assessed using clinical evaluation methods and electrophysiological examinations, as well as retrograde labeling and axonal counting assessments of the reconstructed nerve pathways.Results: The evaluations show that the remaining facial axons not only influenced the extent of regained function, such as facial symmetry, eye blinking activity, and vibrissae motion, but also had an impact on regeneration and innervation of hypoglossal motoneurons.Conclusion: Participation of remaining or spontaneously regenerated facial axons plays an important role in innervating paralyzed facial muscles by both facial and hypoglossal motoneurons, thus, reestablishing facial function.
Highlights
Facial nerve (FN) injury frequently results from cranial trauma, tumor, inflammation, or surgery at the cerebellopontine angle area, inducing either complete or incomplete permanent or transitory facial paralysis
We modified the classical method of HNFN side-to-end neurorrhaphy by side-to-side to preserve the remaining FN fibers and the possibility of spontaneous regrowth of the FN, showing that innervations of both HN and FN fibers could be achieved with the return of certain facial functions [2, 3]
We hope that this study provides useful information for neurosurgeons to determine the method of HN-FN neurorrhaphy for treating anatomical structure-preserved FN injuries
Summary
Facial nerve (FN) injury frequently results from cranial trauma, tumor, inflammation, or surgery at the cerebellopontine angle area, inducing either complete or incomplete permanent or transitory facial paralysis. The incidence of incomplete facial paralysis is relatively higher clinically In those cases, surgical intervention is still desirable for patients with significant incomplete facial paralysis, such as with House–Brackmann (H-B) grade IV or V on FN function [1]. Surgical intervention is still desirable for patients with significant incomplete facial paralysis, such as with House–Brackmann (H-B) grade IV or V on FN function [1] This issue raises the question of how to address the injured FN when using hypoglossal–facial nerve neurorrhaphy (HN-FN) or other nerve transfer methods. The importance and usefulness of the remaining and/or spontaneously regenerated facial axons for regaining facial function when using hypoglossal–facial nerve (HN-FN) neurorrhaphy or other nerve-transferring methods to treat facial paralysis remain controversial
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