Most patients with primary facial muscle spasm develop after middle age, with more women. At the beginning of the course of the disease, it is mostly paroxysmal involuntary twitching of the orbicularis oculi muscle on one side, which gradually and slowly extends to other facial muscles on one side of the face, and the twitching of the corners of the mouth muscle is most easily noticed. The degree of twitching varies, and it is paroxysmal, rapid and irregular twitching. The initial twitch is light and lasts for only a few seconds, and then gradually grows for several minutes or longer, while the interval is gradually shortened and the twitches gradually increase in frequency. In severe cases, it is tonic, causing the ipsilateral eye to be unable to open, the corner of the mouth to be skewed to the ipsilateral side, and the inability to speak, often aggravated by fatigue, nervousness, and voluntary movement, but it cannot imitate or control its seizure by itself. A convulsion can last from a few seconds to more than 10 minutes, with intervals of variable length. The patient feels distracted and unable to work or study, which seriously affects the patient’s physical and mental health. Most of the convulsions stop after sleep. Bilateral lateral muscle spasms are rarely seen. If there is, it often starts on both sides successively, and most of the convulsions stop on one side, then the other side has another attack, and the convulsions are light on one side and light on the other side, and the simultaneous onset and convulsions on both sides have not been reported. A few patients have mild facial pain during convulsions, and individual cases may be accompanied by ipsilateral headache and tinnitus. Grade 0: no spasm; Grade 1: increased transients or mild facial muscle tremors caused by external stimuli; Grade 2: spontaneous mild tremors of eyelids and facial muscles with no dysfunction; Grade 3: pronounced spasm with mild dysfunction; Grade 4: severe spasm and dysfunction, such as the patient being unable to read or walk alone because of the inability to open the eyes continuously. Neurological examination was not positive for signs other than paroxysmal twitching of facial muscles. A small number of patients may have mild paralysis of the affected facial muscles in the late stage of the disease. Treatment of facial spasm I. Drug therapy Except for phenytoin sodium or carbamazepine, which may be effective in some mild patients, general central sedatives, depressants and hormones have no significant effect. In the past, procaine, anhydrous alcohol or 5% phenol glycerin were commonly used to do injections at the stem mammary foramen to cause transient necrotic degeneration of nerve fibers and reduce abnormal excitation conduction, with a single injection of 0.3-0.5 ml to reach to the degree of mild facial paralysis. Injection method: The patient should lie on his side, disinfect the affected subauricular mastoid with alcohol and iodine, disinfect the affected subauricular mastoid with a 20-21 gauge needle at the junction of the cartilage at the base of the external auditory canal and the anterior border of the mastoid, connect a 2ml syringe with the tip of the needle pointing upwards in front and at an angle of 30 degrees with the horizontal line of the skull base, pierce 3cm into a depression, inject 1ml of 1% procaine first, do not pluck out the needle, observe whether facial paralysis appears for 1 to 2 minutes, if If facial palsy appears, it means that the nerve stem is hit, and then an empty needle with water and alcohol is attached and 0.3~0.5ml of alcohol or phenol glycerin is injected, and obvious facial palsy will occur and the spasm will disappear. After half a year, facial paralysis can be gradually recovered, and about 2/3 of patients will have a recurrence of spasm. Radiofrequency temperature-controlled thermocoagulation therapy The radiofrequency cannula needle is stabbed into the stem mammary foramen according to the above method, and using the principle of electric coupling, heat is generated between nerve fibers by radiofrequency, and the temperature is 65～70℃. Under the supervision of facial nerve function monitor, the temperature is controlled to make the nerve thermocoagulated and denatured to reduce the nerve fibers that conduct abnormal impulses. The same facial palsy should occur after surgery, and the old disease will recur during the gradual recovery of facial palsy in 1 to 2 years, otherwise the electric heat is excessive, and although the spasm can be long-term without seizure, it will be replaced by permanent facial palsy. Third, surgical treatment Intracranial apparent microvascular decompression. Under general anesthesia, the suboccipital or posterior sigmoid sinus pathway is used, the occipital bone is excised to make a 3×4 cm bone window, the meninges are cut, the pontocerebellar angle is entered, the VII and VIII cranial nerves are identified, and if any occupying lesions or arachnoid adhesions are found, they are excised and decomposed, and if there are compressive vessels, they can be separated under the microscope with microscopic instruments. Muscle sheets can also be used to fill in between the vessels and the nerves. These vessels are mostly trips of the anterior inferior cerebellar artery, which is the main blood supplier to the brainstem. There is a significant preoperative and postoperative difference, and the symptoms are completely eliminated after surgery.