Facial spasm is customarily called “facial twitching” and is characterized by episodic and recurrent involuntary twitching of the facial muscles. According to statistics, the incidence of this disease accounts for 6/400,000 to 180,000/100,000, and patients with this disease may be found when walking in the street with a little attention. The youngest patient treated at our hospital was 14 years old, and there was no significant difference between men and women in terms of gender ratio. The clinical manifestations of DD facial muscle spasm have distinctive features. The majority of facial muscle twitches are limited to one side, often occurring first in the eyelid, similar to eyelid jumping, and then gradually expanding in scope, mostly spreading to other facial muscles, the corners of the mouth, and even the broad neck muscles after a few months. There is no aura before the attack, and the attack is characterized by rapid and frequent muscle twitching for a few seconds to a few minutes each time, and everything is as normal in the interval. Autonomous facial movements, chewing, transient eyes or random facial expressions can trigger facial muscle twitches, which can be aggravated by emotional excitement, stress, exertion or prolonged reading time, and the symptoms are reduced when resting or emotionally stable. If the seizure is serious, it can be twitching all day long, even during sleep. In some patients, the eyelid fissures may become smaller due to compulsive contraction of the eyelids, and in some patients, even the facial muscles may contract tensely, causing the corners of the mouth to be continuously tilted to the side of the disease. The disease has a chronic course and can extend for life, which has a great impact on the work, mental and life of patients. Individual patients with facial twitches may have trigeminal neuralgia (about 0.8% of patients with facial twitches). In addition, some patients may also have tinnitus, vertigo, and hearing loss on the affected side. The disease is not hereditary or contagious. Clinical examination: Apart from involuntary facial twitching, patients with facial muscle twitching usually have no obvious positive features. A few patients may show incomplete facial muscle paralysis because they have been treated with botulinum toxin injection, acupuncture, closure or radiofrequency thermal coagulation, facial nerve combing and other injurious treatments. Long-term patients may develop atrophy of the affected facial muscles. 99.1% of facial muscle spasms are caused by intracranial vascular compression of the facial nerve root. 99.1% of patients with facial muscle spasms used to be called primary facial muscle spasms, whose etiology is due to compression of the facial nerve root by abnormal blood vessels in the outgoing pontocerebral segment (the segment of the facial nerve just emanating from the brainstem), causing damage to the facial nerve and demyelination, resulting in a current ” short circuit” between nerve fibers “, which triggers facial muscle twitching. In recent years, a large number of clinical practices have also shown that once the compression of the nerve root by blood vessels is removed, facial muscle spasm can be stopped immediately or gradually. At present, the etiological theory that facial muscle spasm is caused by compression of the facial nerve root by blood vessels has been recognized worldwide. Since the cause of facial myospasm is intracranial, the only way to cure the disease is to treat the root of the disease. Secondary facial myoclonus refers to the presence of clear predisposing diseases, such as peripheral facial palsy caused by facial nerve trauma or facial neuritis, which can cause facial muscle associated movement during the recovery period with characteristics similar to facial myoclonus; some tumors or inflammation of the pontocerebellar horn involving the facial nerve root can also cause the occurrence of this disease. Statistically, except for facial spasms after traumatic facial paralysis, other secondary facial spasms account for only 0.9% of all facial spasms. Almost all facial muscle spasms begin with eyelid fluttering, and simple eyelid fluttering (medically called blepharospasm) is extremely common in daily life and is experienced by almost everyone in their lifetime. In folklore, there are some superstitious legends about eyelid jumping, such as “left eye jumping for money, right eye jumping for disaster”. Simple eyelid jumping is caused by focal excitation of the nerve muscles that govern eyelid movement, and this condition mostly resolves on its own after a period of time. In the case of facial spasms, the eyelid spasms do not stop on their own, but get heavier and heavier, gradually involving the facial muscles and even the neck and shoulder muscles after a period of jumping. Therefore, it is important not to rush to seek medical attention after the onset of blepharospasm, because simple blepharospasm does not develop into facial muscle spasm. In the case of facial muscle spasm, general treatment cannot stop the natural course of the disease, in which the facial muscle twitching gradually worsens. In addition, facial myospasm has to be differentiated from hysterical blepharospasm, habitual facial twitching, and restrictive epilepsy. Microvascular decompression is currently the only cure for facial myasthenia There are no specific drugs for facial myasthenia. In the past, various destructive methods have been used to treat the disease by causing partial paralysis of the facial muscles, such as drug closure, percutaneous percutaneous facial nerve radiofrequency thermal coagulation, facial nerve combing or its branches, major trunk severance, intracranial facial nerve root extrusion, partial nerve injury in the facial nerve canal, etc. The only effective method of internal treatment is the closure of the trunk or branches of the facial nerve with botulinum toxin, which stops the facial muscle spasm by causing partial or complete paralysis of the facial muscle, but the effect lasts only 3 to 6 months, and repeated injections may cause permanent facial paralysis. Patients with blepharospasm and facial spasm should choose the right treatment to avoid unnecessary financial costs and new pain. In 1967, Professor Jennatta pioneered the microvascular decompression procedure for facial myasthenia gravis. The method is to drill a 1.5-2.0 cm diameter bone hole behind the affected ear, expose the facial nerve root under a microscope, find the blood vessel compressing the facial nerve root and then free it, and use Teflon cotton to pad the compressing blood vessel away from the nerve. Since the 1980s, this procedure has become the preferred treatment for facial spasm internationally, and to date, more than 50,000 patients worldwide have been treated for facial spasm. The overall cure rate worldwide is between 82% and 99%, and the recurrence rate is only about 1-5%. Theoretically, the cure rate of this surgery should be close to 100%, but the main reason for this difference in efficacy is the experience of the surgeon, whose inexperience may result in the omission of the responsible vessel, the incorrect position of the Teflon pad leading to insufficient decompression; secondly, because the blood vessel compressing the facial nerve root is too large, it is difficult to perform effective decompression with the current decompression method. Since this surgery is minimally invasive, it requires high microsurgical skills of the operator, and the safety, complication rate and efficacy of the surgery are mainly determined by the experience of the operator. Generally speaking, the operator must have accumulated more than 500 cases of surgical experience in order to achieve a high level of surgical efficacy and to reduce the complication rate to a low level. The most common complication of this procedure is hearing impairment, with an incidence of 2% to 5% and a serious complication of less than 1/1000. Therefore, microvascular decompression is a safe procedure.