Hemifacial spasm (HFS), also known as facial muscle twitching, is an involuntary seizure in which the main symptom is twitching and contraction of one of the facial muscles. It can be triggered by emotional stress, anger and light stimulation, and is progressive in development. In severe cases, severe spasms can significantly disfigure the face. There are no other positive neurological signs, while the EEG is normal and the EMG shows myofiber tremor and myofascicular tremor waves. The incidence rate is 0.78/100,000. The incidence is 0.78/100,000. It is more likely to occur after middle age. Guo Qiang, Department of Neurosurgery, Shenzhen Hospital, Peking University, Beijing, China The concept of vascular compression was first proposed by Schuhze in 1875 and Gardner in 1960, who also believed that vascular compression led to reversible demyelination of facial nerve roots, which in turn caused short-circuiting between neurons and eventually led to spasticity. In 1975, Jannetta first confirmed by pathological and histological examination that vascular compression caused demyelination of nerve roots and degeneration of facial neurons as the main basis for the pathogenesis. In the 1980s, Kim and Nielsen proposed a new theory that vascular compression caused contact between nerve fibers, resulting in ectopic excitation, allowing nerve conduction to spread between different fibers, which is the reason for the synergistic movement of the periocular and cheek muscles in most patients. To date, there are two main hypotheses for the pathogenesis of facial spasm. 1. Proponents of this theory believe that the REZ region of the facial nerve is unmyelinated and is surrounded only by oligodendrocytes. Due to the prolonged vascular compression of this segment, ectopic impulses are generated across the exposed axons by synaptic transmission. 2. Scholars engaged in electrophysiological research believe that the REZ area of the facial nerve is compressed by blood vessels and generates reverse impulses, thus “igniting” the facial nucleus, and with the increase in excitability, the muscle develops involuntary movements. Currently, the “nucleus accumbens” theory is becoming more and more accepted, and it can explain some problems that cannot be explained by the “short circuit” theory. Despite this, the pathogenesis of facial spasm is still unknown, but it has been clinically found that compression of any part of the facial nerve from the pontine sulcus to the internal auditory meatus may lead to the development of facial spasm, and the contact between the vessel and the facial nerve root may be an important condition for the development of facial spasm. Although there are various methods of treatment for facial myospasm, there are three main methods with certain clinical efficacy: pharmacotherapy, local injection of Botulinum toxin A (Botulinum toxin A) and microvascular decompression surgery (MVD) of facial nerve. 1. Pharmacotherapy: commonly used drugs include carbamazepine (Deltamethrin), oxcarbazepine, phenytoin sodium, sodium valproate, clonidine, baclofen, etc. Baclofen, etc. However, the biggest problem of drug therapy is that all spasticity symptoms can only be temporarily relieved or reduced, but not completely cured, and at higher doses there are complications of hematopoietic and xerophrenic damage, and some patients often have allergic reactions. This has severely limited the widespread use of drug therapy. Currently, drug therapy is mostly used for patients with initial spasms or mild spasticity, and sometimes as an adjunctive treatment for patients whose symptoms cannot be completely relieved after surgery. 2. Botulinum toxin A local injection therapy: Botulinum toxin is a neurotropic protein that blocks the conduction of neuromuscular junction. The duration of action of different types of botulinum toxin varies, but the main clinical application is botulinum toxin A. After a latent period of 2-5 days after subcutaneous injection of botulinum toxin, it is reported in the literature that the symptoms of muscle spasm in the area of botulinum toxin injection can be completely disappeared or significantly reduced in more than 75% of patients, and the duration of efficacy depends on the dose of botulinum toxin injection, which can be maintained for several months. The duration of the effect depends on the dose of Botox injections, and most of them can last for several months, and repeated injections can still achieve satisfactory results. Botox injections are often accompanied by dry eyes, tearfulness, diplopia, weakness of the eyelid and cheek muscles, and even permanent paralysis of some of the cheek muscles after multiple injections. In addition, the efficacy of Botox injections is temporary, and maintaining the efficacy requires regular and repeated injections, which not only cannot cure facial muscle spasm, but also consumes considerable medical expenses. This not only does not cure facial spasm, but also consumes considerable medical costs. This has largely limited the widespread use of botulinum toxin. At present, botulinum toxin injection therapy is mainly used for patients who are not treated with medications and lack of surgical conditions, and it can also be used as a supplementary treatment option for patients who are not effective after surgery. 3. microvascular decompression (MVD): the responsible vessels compressing the facial nerve are freed and pushed away to place spacers to isolate them. With the application of the surgical microscope in clinical practice, Jannetta took the lead in refining and standardizing the theory and surgical technique of microvascular decompression, and popularized the surgical technique internationally. It has been widely performed worldwide. The literature reports that postoperative ineffectiveness ranges from 2% to 13% of patients, postoperative recurrence from 8% to 20%, and postoperative complication rates of 6% to 19%.