Effects of Edaravone on Recovery of the Facial Nerve After Crush Injury: Original Study-Brief Clinical

In traumatic peripheral facial nerve paralysis, the risk of permanent sequelae remains high despite current surgical and medical treatments. Edaravone is a free radical scavenger with antioxidant and antiapoptotic properties; however, its efficacy in facial nerve injury has not yet been established. This study aimed to evaluate the effect of edaravone on facial nerve recovery following crush injury in a rat model. Thirty rats were randomly assigned to 3 groups (n=10 per group): group 1 (saline-treated control), group 2 (methylprednisolone-treated), and group 3 (edaravone-treated). Facial paralysis was induced by compressing the right facial nerve trunk using a standard mosquito clamp. Whisker movements and eye-blink reflexes were evaluated weekly for 4 postoperative weeks and compared with those of the contralateral, unaffected side. Histopathologic evaluation included measurements of axon diameter, myelin sheath thickness, and nerve fiber diameter. Schwann cell apoptosis was assessed using a terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay. Significant differences in eye-blink reflex and whisker movements were observed among the groups at postoperative week 2 (P<0.01). By week 4, the functional scores in the edaravone-treated group did not differ from the preinjury values (P>0.05), whereas functional deficits persisted in the control and methylprednisolone-treated groups (P<0.05). Histopathologic analysis revealed significant differences in nerve fiber diameter and Schwann cell apoptosis (P<0.001). Edaravone demonstrated beneficial effects in this experimental model of traumatic facial paralysis, with functional recovery consistent with the histopathologic findings, suggesting that edaravone may represent a potential treatment option for this condition.