Today, I received another consultation call from a female patient from Guangdong, who has been suffering from facial paralysis for one year and one month, and has been treated with medication in various hospitals, with unsatisfactory recovery, and has facial hypermobility (sequelae of facial paralysis). Such a patient is encountered from time to time, and I don’t know how many of them I have encountered. Unfortunately, it would have been possible for her to get a better result. It is necessary to talk about the misconceptions of facial palsy treatment in the hope that more patients will receive scientific treatment. Most causes of facial palsy are due to facial neuritis caused by cold or viral infection. The facial nerve is the longest nerve in the body that travels in the bones. It comes from inside the skull to outside the skull through a long bone canal in the temporal bone, and then sends out branches to distribute in the face, mainly managing the movement of facial muscles. Facial neuritis will cause facial nerve edema, and the pressure inside the bone canal in the temporal bone will rise sharply, further causing facial nerve ischemia and hypoxia, further aggravating edema and causing nerve fiber necrosis in severe cases. The early treatment of facial palsy is mainly hormonal (e.g. prednisone, dexamethasone) anti-edema, supplemented by anti-viral drugs (e.g. aciclovir). If the symptoms do not improve after two weeks, or if the disease progresses rapidly, although less than two weeks, the electromyogram shows most of the nerve (e.g. 90%) function loss
Surgery should be performed to grind open the bone canal in the temporal bone to fully expose the facial nerve, so that the facial nerve can be fully decompressed, improve the blood circulation of the facial nerve, reduce edema, prevent nerve necrosis, and create conditions for nerve regeneration.