Facial muscle spasm, also known as facial muscle twitching, is characterized by paroxysmal painless involuntary spasmodic contractions of the hemifacial muscles, usually limited to one side of the face, and occasionally seen bilaterally. At the beginning of the disease, it is mostly paroxysmal involuntary twitching of one eye muscle (especially the lower eyelid), which gradually and slowly spreads to the ipsilateral cheek, corner of the mouth and other hemifacial muscles twitching at the same time, and in severe cases, it may involve the ipsilateral broad muscle twitching of the neck. The disease may be accompanied by weakness of the affected lateral muscles or mild facial paralysis in advanced stages. The disease is slowly progressive and usually does not improve or disappear on its own, affecting the patient’s appearance and causing great inconvenience to daily life and work. The vast majority of facial spasms are idiopathic (also called primary), and very few are secondary to intracranial tumors, aneurysms, vascular malformations, cysts, sarcoidosis, and other lesions. Studies have shown that lesions in the intracranial segment of the facial nerve near the brainstem caused by vascular compression are the root cause of facial spasm. Treatment includes medication, facial nerve closure method and surgery. Medications are usually given as sedative drugs such as Valium and Phenobarbital, which generally have no significant effect. Facial nerve closure method is to use alcohol, botulinum toxin A, etc. to close the trunk or branches of the facial nerve, which is relatively simple and convenient, but can cause incomplete facial paralysis, the recent effect is good, the efficacy is short-lived, and often requires repeated injections of closure. After years of practice and improvement, neurosurgical microvascular decompression for “vascular compression” has become the safe and effective method of choice for the treatment of facial muscle spasm. Patients diagnosed with facial myasthenia gravis without systemic organic lesions such as severe cardiovascular disease can be considered for microvascular decompression treatment. The procedure is performed under general anesthesia with a minimally invasive “locking hole” craniotomy under the occiput behind the affected ear, exposing the near brainstem segment of the facial nerve under a microscope, finding and identifying the “compressed vessel”, and lining it with myofascial or Teflon sheets until the EMG is induced. Until the abnormal myopotential changes disappear and the decompression is confirmed to be adequate. The incision will be discharged in 7 days after the incision is removed. The overall efficiency of this procedure for the treatment of facial myoclonus can be about 95% in experienced neurosurgical centers. Postoperatively, patients may experience transient headache, dizziness, nausea, vomiting, and fever, most of which can disappear within a week. The mortality and complication rates of the procedure are extremely low.