acial palsy is a devastating clinical condition that hinders affected individuals' appearance, function, communication, and overall quality of life. [1][2][3] There are significant psychosocial morbidities associated with facial palsy and associated smile asymmetry. [4][5][6] Nonflaccid facial palsy develops 6 to 18 months after in-continuity facial nerve insults and is characterized by zonal synkinesis, hypertonicity, and hypomobility. 7 Common causes of nonflaccid facial palsy include Bell palsy, Ramsay Hunt syndrome, acoustic neuroma resection, trauma, Lyme disease, and autoimmune disease. The leading cause of nonflaccid facial palsy is Bell palsy, 8,9 with an incidence of 25 to 35 cases per 100,000, 10 15 to 30 percent of which will suffer from nonflaccid facial palsy. 11 Facial nerve repairs, including neurorrhaphy, nerve grafting, and nerve transfer, can also result in nonflaccid facial palsy. [12][13][14] Although there are multiple theories explaining the development of nonflaccid facial palsy, the most widely accepted theory is that regenerating axons extend in multiply terminal