Objective: The protective effect of edaravone, an inhibitor of reactive oxygen species (ROS), against the development of ischemia-induced facial palsy was investigated.
Methods: Experimental ischemic facial palsy was induced by interruption of the petrosal artery (PA) in guinea pigs. The application of edaravone was carried out by daily intraperitoneal injection for 1 week. The behavioral facial movement, fluorescence intensity of ROS, and morphological changes were investigated.
Results: Edaravone injection from immediately after PA interruption significantly reduced dihydrotetramethylrosamine fluorescence intensity (indicative of ROS) in the facial nerve of the interrupted ear and attenuated the development of ischemia-induced facial palsy. Edaravone injection from the 2nd day following PA interruption also reduced the incidence of facial palsy. Light and electron microscopy revealed that edaravone application tended to prevent the degenerative changes of the facial nerve caused by ischemia.
Conclusions: Edaravone suppressed the production of ROS and had a remarkable protective effect against the development of mild to moderate facial palsy. Morphologically, nerve damage was also decreased by edaravone injection.