Facial myoclonus, also known as facial twitching and hemifacial spasm, manifests as episodic, rhythmic involuntary twitching of one side of the facial muscles. The incidence of the disease is 1 per 100,000, mostly seen in middle-aged and elderly people, and the cause of the disease is still unknown. In terms of the causative mechanism, the “nerve short circuit” theory is now recognized by clinicians, based on the fact that the intracranial facial nerve from the brainstem is compressed by the abnormal vascularity of the vertebrobasilar system, and the facial nerve is pathologically stimulated to produce abnormal nerve impulses, resulting in facial muscle twitching. In terms of clinical symptoms, the spasms mostly start from the lower eyelid on one side and gradually spread to the face and even the neck muscles. When the twitching is severe, it can cause facial pain and affect vision, speech and sleep. Since the cause of facial muscle spasm is the compression of the root of the facial nerve by the abnormal vascularity, and the anatomical structure and function of the facial nerve and vascularity are normal, there are no other abnormal findings in physical examination except for the involuntary twitching of one side of the facial muscle paroxysm. In terms of special examination, CT or MRI scans of the head can show abnormally shaped blood vessels at the root of the facial nerve in some patients, but there are no other abnormal findings. The former includes oral medication and drug injection facial nerve block therapy, there is no special oral medication, some sedative and tranquilizing drugs are commonly used in clinical practice; nerve block therapy is to use botulinum toxin and ethanol to block the conduction function of facial nerve, so that facial muscle spasm can be released. After injection, the nerve conduction is impaired and the facial muscle is immediately paralyzed or incompletely paralyzed, and such facial muscle paralysis can be recovered within a few months. The effect is short-lived, and most patients relapse in about 3-6 months and need to be treated by injection again. Common complications include facial palsy, dry eyes, diplopia, and dysphagia. Other surgical methods are rarely used due to poor treatment effect and high surgical complications. Microvascular decompression was pioneered by an American neurosurgeon in the late 1960s. The surgical method is to push away the blood vessels that are located at the root of the facial nerve and cause compression on the facial nerve under the operating microscope, and fix them so that they do not touch the facial nerve, thus relieving the compression on the root of the facial nerve, restoring the normal function of the facial nerve, and relieving the symptoms of facial muscle twitching. With the perfection of this surgical technique, especially its characteristics of minimally invasive, high safety, remarkable effect and low recurrence rate and complications, especially the ability to completely preserve the function of blood vessels and nerves, it was soon accepted by neurosurgeons all over the world and promoted worldwide, becoming the most effective treatment for facial muscle spasm. In addition, manifest microvascular decompression has been successfully used to treat trigeminal neuralgia, glossopharyngeal neuralgia, as well as intractable vertigo, tinnitus, neurogenic hypertension, and spastic diastasis. The procedure is performed under general anesthesia and is painless for the patient. The surgical incision is made in the hairline behind the affected ear, about 3-5 cm long, and a small hole of 1.5 cm in diameter is drilled in the skull.