Peripheral facial nerve palsy is a common clinical condition that manifests as a tilted mouth and eyes and can have a variety of causes. Common causes of peripheral facial palsy include Bell’s palsy, facial palsy due to herpes zoster of the ear (Ramsay-Hunt
Syndrome), temporal bone fracture, otitis media, and surgical injury. Examination of peripheral facial palsy: Signs and symptoms: loss of frontal lines, inability to close eyelids completely, loss of nasolabial folds, deviation of the corners of the mouth; deviation of the corners of the mouth when teeth are bared and inability to puff. There is food retention on the side of facial palsy when eating; inability to speak for a long time and other symptoms. Sometimes there are symptoms such as dry eyes and loss of sense of taste. The focus is on understanding the time of the patient’s symptoms and the process of change; whether the degree of facial palsy is complete or incomplete facial palsy; whether it is accompanied by hearing loss, vertigo and other symptoms; time is the key to treating facial palsy and trying to make a judgment before the facial nerve damage becomes irreversible. The diagnosis of facial palsy includes both localization diagnosis and qualitative diagnosis. Auxiliary examination (qualitative examination): The most commonly used diagnostic methods are: neuroelectrogram and electromyogram, etc. Neuroelectrogram: It is an evoked potential that provides an objective basis for the degree of nerve degeneration and mainly provides the percentage of degenerated motor fibers. The prognosis for Bell’s facial palsy is poor if the degeneration is 95% or more within 14 d after the onset of the injury. A degeneration percentage of 90% to 94% is an important indication for emergency surgery. Evoked potentials are only applicable when the myopotentials are superimposed synchronously. Facial muscle movements occur when physiological conduction block is recovered, while evoked potentials may not recover because evoked pulses are asynchronous and the myopotentials are not superimposed properly. Electromyography: It is difficult to determine the prognosis of early facial palsy by electromyography alone. Loss of nerve muscle potential is seen 14 to 21 days after the onset of complete facial palsy, indicating that the nerve damage is irreversible and decompression has lost its significance. Loss of nerve potential due to trauma is an indication for surgical exploration. EMG combined with evoked potentials is particularly useful in the following cases: muscle contractions are not detectable by the naked eye, but active motor units can be recorded, indicating that the nerve damage is not severe; severe degeneration does not occur when active motor units persist for up to 7 d after the onset of facial palsy.