The incidence of facial muscle spasm, also known as facial muscle twitching, is 1 per 100,000, mostly seen in the middle-aged and elderly population. In terms of pathogenesis, the “nerve short circuit theory” is now recognized by clinicians, mainly manifesting as episodic, non-random twitching of the muscles innervated by the facial nerve, most often involving the eyelids (eyelid jumping), but also involving the cheek and corner of the mouth muscles, the eye fissure on the affected side shrinks when the attack is severe, and the corner of the mouth is distorted by pulling. It often occurs during fatigue or stress, and often decreases or disappears during quiet and sleep. Facial spasm can be divided into two types: primary and secondary: primary facial spasm accounts for the majority. The majority of primary facial myospasms are due to compression of the facial nerve out of the brainstem by abnormal walking vessels. Secondary facial myoclonus is less common and can be due to tumors, hemangiomas, cysts, trauma in the pontocerebellar horn region, or due to lesions such as brainstem encephalitis. It is often accompanied by other symptoms of cranial nerve damage. The intensity of facial spasticity is graded according to that developed by Cohen et al. Grade 0: no spasm; Grade 1: increased transients or mild tremors of facial muscles caused by external stimuli; Grade 2: spontaneous mild tremors of eyelids and facial muscles without dysfunction; Grade 3: pronounced spasm with mild dysfunction; Grade 4: severe spasm and dysfunction, e.g., the patient is unable to read and has difficulty walking alone because he cannot keep his eyes open. Neurological examination is 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. Facial muscle spasm common treatment methods: 1, drugs: commonly used carbamazepine, clonazepam, baclofen, sedative drugs, but in most cases the efficacy is poor, and side effects. 2, botulinum toxin injection: botulinum toxin injection can only obtain short-term results, generally 3 to 6 months relapse, repeated injections are required, some patients repeatedly injected effect gradually faded, and can appear eyelid drooping, nasolabial folds shallow, drooping corners of the mouth and other symptoms. 3, microvascular decompression: microvascular decompression is currently the internationally recognized method of choice for the treatment of primary facial myasthenia, with a postoperative efficiency of about 98% and a recurrence rate of about 5%. The surgery is performed under a microscope, within the hairline behind the patient’s ear, with an incision of about 4-5 cm in length. A small bone window of about 2 cm in diameter is simply made behind the mastoid process, and after finding the blood vessels compressing the facial nerve, the relevant vessels are separated from the nerve and appropriate material is padded between them. The safety factor of the surgery is high, and most patients can recover as normal after surgery, but a very small number of patients will have complications such as facial palsy, tinnitus, hearing loss, infection and bleeding to varying degrees, and the mortality rate is very low or close to zero, about 0.5% or less. In summary, facial nerve microvascular decompression is currently the only method that can cure primary facial spasm with good efficacy and high safety factor, and most patients can be cured. However, botulinum toxin injection therapy is still recommended for patients with other contraindications to surgery, such as serious heart, liver, lung, and kidney diseases.