Abstract
Objective: Examine the effect of both local and systemic dexamethasone administration on facial nerve return of function after complete axotomy and immediate microsurgical repair in a rat model. After nerve injury, an exaggerated neuro-inflammatory process may hinder regeneration. Therefore, our hypothesis is that glucocorticoid administration will improve nerve recovery. Method: A total of 74 Wistar rats underwent facial nerve axotomy with immediate neurorrhaphy. Blinded and randomized, rats were assigned a postoperative group: control (no therapy), systemic dexamethasone 0.5, 1, 5, or 10 mg/kg for 3 doses, or topical dexamethasone 2 or 4 mg/mL. Standardized facial assessments and nerve conduction studies (NCS) were performed. Results: At 8 weeks, rats receiving systemic dexamethasone at 1 and 5 mg/kg attained greater eye blink closure ( P = .014 and P = .018, respectively) and vibrissae motion ( P = .018 and P = .023, respectively) compared with controls. Systemic dexamethasone at 0.5 and 10 mg/kg had similar facial motion to controls. Intraoperative topical application of dexamethasone 2 or 4 mg/mL to the neurorrhaphy site was not superior to controls. Gross facial motion assessments were corroborated with vibrissae motion frequency video analysis. NCS’s indicated an increased return of compound muscle action potential amplitude levels to baseline among rats that received systemic dexamethasone 5 mg/kg ( P = .048). Conclusion: In a rat facial nerve axotomy model, postneurorrhaphy systemic dexamethasone therapy improved functional and neurophysiological outcomes at doses of 1 and 5 mg/kg. Locally delivered steroid was not beneficial compared with control groups. Therefore, systemic glucocorticoid administration may provide a substantial recovery benefit after facial nerve injury.
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