Hemifacial spasm (HFS), also known as facial muscle twitching, is usually confined to one side of the face, hence the name hemifacial spasm, and can occasionally be seen on both sides. It is a recurrent involuntary twitching, or even spasm or tonic seizure of the facial muscles innervated by the facial nerve; the onset of the disease starts from the orbicularis oculi muscle and gradually extends downward to the orbicularis oris muscle and facial expression muscle. It can be aggravated by fatigue and tension, especially when speaking and smiling, and in severe cases it can be spastic. When frequent attacks occur, the face is deformed, accompanied by tightly closed eyelids and skewed corners of the mouth, which seriously affects the patient’s image and quality of life. At the end of the development of facial muscle spasm, mild facial paralysis may appear in a few cases. According to epidemiological surveys, the prevalence of facial myasthenia in the population is 20/10,000,000, mostly in middle age, with the youngest age reported to be two years old. In the past, it was thought to be more prevalent in females, but in recent years, statistics have shown that the onset is independent of gender. There are 12 pairs of nerves in the brain, of which the seventh pair is called the facial nerve, which emanates from the pons and mainly governs the activity of facial muscles. In the early 1990s, a professor at the University of Tokyo in Japan discovered that the cause of the disease was due to abnormalities in the course of intracranial blood vessels compressing the facial nerve. Due to the presence of anatomical variants and the hardening of intracranial vascular tortuosity with age, the compression of the facial nerve root into the brainstem causes the nerve fibers to squeeze together, resulting in localized damage to the nerve fibers, which then undergoes demyelination. Pseudosynaptic transmission occurs between adjacent afferent and efferent nerve fibers, i.e., a “short circuit”. A slight tactile stimulus can form a series of impulses that pass through the “short circuit” to the center, and the efferent impulses from the center can also become afferent impulses through the “short circuit”, so that a certain “sum” is quickly reached. “until the neurons involved in this process are exhausted. After an interval of varying length, the above process is repeated again, so that repeated involuntary twitching of the facial muscles occurs. The cause of the disease is intracranial, and it is difficult to achieve good results with various external local treatments. Therefore, the ideal treatment is to relieve the compression of the nerves by blood vessels while completely preserving the function of blood vessels and nerves. Because of the slow progression and long duration of facial spasm after the onset of the disease, there is generally no automatic remission trend, and the drugs used for treatment include: methylcobalamin capsules, carbamazepine, and thiopride hydrochloride (benzamide antipsychotics, which are effective in sensorimotor neurological disorders and psychomotor behavior disorders). Although some patients are treated with botulinum toxin, recurrent relapses of botulinum toxin treatment are not tolerated and conservative treatment is not effective, surgery should be performed as soon as possible. Microvascular decompression of the facial nerve in the posterior cranial fossa is increasingly accepted by more patients because of its efficacy, less susceptibility to recurrence, minimal facial sensory deficits, and, with the development of the surgical microscope, a low incidence of complications. The core principle of this type of surgery is that the blood vessel loops compressing the facial nerve root are separated under the operating microscope, and then a special spacer is inserted to isolate the blood vessel from the nerve, which completely removes the compression of the blood vessel on the facial nerve and relieves the patient’s pain, and is currently the most effective method for facial muscle spasm disease recognized internationally. Microvascular decompression, which has an overall efficiency of 90% in the treatment of facial myospasm and a low recurrence rate, has brought light to patients with facial myospasm. Indications for facial myospasm: 1. primary HFS, onset for more than half a year, ineffective by medical treatment or continues to worsen, affecting normal life and interaction, with a request for surgical treatment. 2. no history of facial nerve injury. 3. exclude more serious systemic diseases such as more serious liver, kidney, cardiovascular disease, and able to tolerate this procedure. 4. exclude the presence of bleeding disorders and bleeding factors. The patient was 39 years old and had been taking carbamazepine and thiopride hydrochloride for 6 years. “The patient’s recurrent involuntary twitching of the facial muscles disappeared. Facial muscle spasm with trigeminal neuralgia There is a regular chronology of the onset of facial muscle spasm and trigeminal neuralgia. The vast majority of patients experience facial muscle spasm first, followed by trigeminal neuralgia, which may be related to the tortuous sclerosis of the vertebrobasilar artery. The connection site of the vertebrobasilar artery is often in the pontine sulcus, which is closer to the facial nerve, and it is easy to compress the facial nerve first and cause facial muscle spasm. With the development of arteriosclerosis and the different degrees of brain atrophy that occur with age, the twisted and sclerotic vertebrobasilar artery may also compress the trigeminal nerve and cause trigeminal neuralgia.