Facial nerve neurorrhaphy and the effects of glucocorticoids in a rat model

After nerve injury, an exaggerated neuroinflammatory process may hinder neuron regeneration and recovery. Immunomodulation using glucocorticoids may therefore improve facial nerve injury outcomes. This study aims to examine the effect of both local and systemic dexamethasone administration on facial nerve functional recovery after axotomy in a rat model.

Randomized, placebo-controlled, blinded animal study. Setting Animal laboratory.

Seventy-four Wistar rats underwent facial nerve axotomy with immediate neurorrhaphy. Rats were randomly assigned a postoperative group: control (no therapy); systemic dexamethasone 0.5, 1, 5, or 10 mg/kg for 3 administrations; or topically applied dexamethasone at 2 or 4 mg/mL. Blinded, standardized facial assessments and nerve conduction studies (NCS) were performed. Gross facial motion assessments were corroborated with vibrissae frequency video analysis.

At 8 weeks, rats receiving systemic dexamethasone at 5 mg/kg attained greater eye blink closure (P = .004) and vibrissae motion (P = .012) compared with controls. Systemic dexamethasone at 0.5, 1, and 10 mg/kg and intraoperative topical application of dexamethasone at 2 or 4 mg/mL did not produce a significant improvement in facial motion compared with controls. Nerve conduction studies show a trend of increased return of compound muscle action potential amplitude levels compared with baseline among rats that received systemic dexamethasone 5 mg/kg but do not achieve statistical significance.

In a rat facial nerve axotomy model, high-dose systemic dexamethasone therapy may improve functional recovery when administered in the immediate period following neurorrhaphy.