Role of the Trigeminal Nerve in Facial Nerve Healing

Introduction: Incomplete understanding of the pathogenesis of aberrant facial nerve recovery is a barrier to developing novel therapies. Prior work has suggested the possibility of interactions between the trigeminal nerve (CNV) and facial nerve following facial nerve injury. This study investigated the hypothesis that CNV branch excision and pharmacologic blockade would impede facial nerve regeneration and axonal guidance.

Methods: Sixty-four female adult Sprague-Dawley rats were divided between two experiments, with all animals undergoing a facial nerve crush injury. In the first experiment, intervention group animals underwent en bloc excision of the infraorbital branch (V2) of the trigeminal nerve at the nasal bridge at time of facial nerve injury. The control group underwent sham surgery to V2, involving identification of the infraorbital branch but no manipulation. In a second experiment, intervention group animals received two injections with liposomal bupivacaine of V2 at time of facial nerve injury, while control animals received no injection. All animals underwent longitudinal functional facial nerve assessment with electromyography (EMG) as well as whisker and eye closure analysis at three time points before harvest. Primary endpoints assessed included facial nerve function, EMG amplitude, and neuro-muscular junction counts.

Results: No significant differences in facial nerve recovery were identified after trigeminal nerve pharmacologic blockage or excision of V2 when compared against controls. Preliminary histopathological analyses involving assessment of neuromuscular endplates and quantitative histomorphometry did not reveal intergroup differences.

Conclusions: A role of trigeminal nerve in facial nerve recovery was not demonstrated. Further investigation is needed to discern whether discrepancies with prior work reflect sensitivity to type of V2 injury and blockade, other differences in model, or limited cranial nerve interaction.