Facial muscle spasm is relatively common in clinical practice, but its etiology is still unclear, and many scholars believe that it is mainly related to the following doctrines. 1, due to some kind of compression of the facial nerve that causes pathological disturbance of its transconduction. Most of the patients are due to normal vascular cross compression, such as posterior inferior cerebellar artery, anterior inferior cerebellar artery, vertebral nerve artery compression, and occasionally due to compression of the facial nerve root by aneurysm, arteriovenous malformation or brain tumor. 2, Another part of patients with idiopathic facial nerve paresis and secondary facial muscle spasm on the affected side after recovery. It may be due to pathological changes in the demyelination of the nerve caused by facial neuritis and failure to restore normal. There is still partial demyelination, which makes the electrical conduction of the facial nerve susceptible to generalization, or facial neuritis involves the nucleus accumbens in the brainstem, forming an epilepsy-like foci and producing seizure-like twitching of the facial muscles. 3. Very few patients develop facial muscle spasms in the affected area after traumatic tumors or surgical procedures. It may be due to short circuit with other brain nerves during the recovery process of facial nerve, and when other nerves are excited, one side of facial muscle twitching also occurs. Clinical manifestations Most patients with primary facial myoclonus develop it after middle age, more often in women. In the early stage of the disease, it is mostly paroxysmal involuntary twitching of the orbicularis oculi muscle on one side, which gradually and slowly expands to other facial muscles on one side of the face. 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 unable to speak, often aggravated by fatigue, mental tension, 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 twitches stop after sleep. Bilateral facial muscle spasms are rarely seen. If there is, it often starts on both sides successively, and most of the convulsions stop on one side, and then the other side has another attack, and the convulsions are light on one side and light on the other side, and bilateral simultaneous onset and convulsions are not 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. Currently, the most commonly used treatments for facial spasm are as follows: ① Surgery: microvascular decompression – the most effective and safe method for treating facial spasm in the world so far. It means that the compression of the nerve by the blood vessel is released under the operating microscope through the locking eye to achieve the treatment purpose. The patient’s convulsions stop immediately after surgery, and the facial nerve function is preserved intact. Clinical symptoms disappear immediately after surgery, and the total effective rate is more than 96%. ② Radiofrequency temperature-controlled thermocoagulation therapy: Using the principle of electric coupling, heat is generated between nerve fibers by radiofrequency at a temperature of 65-70℃, which causes nerve thermal coagulation denaturation to reduce the nerve fibers that conduct abnormal impulses. It is easy to recur after surgery, and even permanent facial paralysis occurs. ③Botulinum toxin injection method: The treatment mechanism is to block the neuromuscular transmission by using botulinum *. Early complete remission is reported to be 80%-100%, but symptoms generally recur after 12-16 weeks and repeat injections are required. Postoperative complications amount to 60-75%. ④ Treatment of patients with facial muscle spasm: the treatment of facial muscle spasm with is not effective, some sedative and tranquilizing treatment, such as phenytoinamide, baclofen, carbamazepine, etc. can reduce the symptoms of a small number of facial muscle spasm.