The surgical treatment of facial neuritis is currently mainly a full decompression procedure via a transcranial middle fossa approach or a combined mastoid approach, which is more commonly used in China. The indications for surgery are mostly based on the facial nerve electrogram (ENoG), and surgery can be considered when the facial nerve electrogram shows >90% nerve degeneration. For the timing of surgery, it is generally not recommended to operate for more than two weeks after the onset of the disease. In 1999, a multicenter prospective study by Gantz et al. found that in patients with severe facial palsy (ENoG facial nerve degeneration >90%), 50%-58% had poor functional recovery with conservative treatment, and 91% of patients with severe facial palsy recovered satisfactorily with decompression of the internal auditory tract, vagus segment, and geniculate ganglion via the middle cranial fossa approach. satisfactorily. Complications of surgery can be seen with hearing loss, conductive deafness, sensorineural deafness, damage to the vestibular system, and permanent facial nerve palsy (anatomical landmarks are unclear, causing irreversible damage to the facial nerve). Infectious injury of the facial nerve, including viral, bacterial, with pathological changes mainly edema, inflammatory cell infiltration, nerve degeneration and hemorrhage, the facial nerve shows diffuse inflammatory demyelination, this pathological process is usually within 40-50 days. The pathological changes in facial nerve compression disease are impairment of forward and reverse axoplasmic transport within the axon and destruction of cell bodies, leading to nerve dysfunction. This compression is an ischemic process with intra-neural edema, elevated pressure, and changes in blood flow within the nerve bundle, resulting in nerve damage. Facial nerve decompression is primarily a treatment for compressive nerve changes and is not therapeutic for infectious local inflammatory reactions. Although microcirculation improves and blood flow is abundant in patients with facial neuritis after surgery, infectious damage still needs time to repair itself. This means that patients with facial neuritis will have another three to six months of recovery after surgery. Note that even with surgical decompression, the vast majority of patients in the multicenter randomized controlled trial data only recovered facial nerve function to House-Brackmann class II, meaning that patients still had visible facial muscle dysfunction. In addition to facial nerve dysfunction, severe facial neuritis also has facial muscle dysfunction innervated by the facial nerve, mainly manifested by centripetal movement of myocyte nuclei and increased satellite cells after loss of innervation. The muscle fibers are significantly reduced in diameter and replaced by rows of adipocytes and connective tissue. Physiological changes: slowed contraction of fast muscles and increased contraction of slow muscles; increased sensitivity of motor endplates to ethylene choline and decreased resting potential. These changes are much less likely to be altered by surgery.