Facial muscle spasm (HFS) is a twitch on one side of the face (individuals appear bilateral spasms), the more nervous and excited the spasm is, the more serious it is. Because the initial symptom of facial myospasm is eyelid jumping, folklore also has “left eye jumping for money, right eye jumping for disaster”, so generally do not attract the attention of people with facial myospasm, after a period of foci formed, the development of facial myospasm, even to the corners of the mouth, serious even with the neck. Facial muscle spasm can be divided into two types, one is the primary type of facial muscle spasm, and one is the facial muscle spasm produced by the sequelae of facial paralysis. The two types can be distinguished by their symptom presentation. In primary facial myospasm, it can occur even at rest, and the spasm is relieved after a few minutes and is not controlled; in facial myospasm produced by the sequelae of facial palsy, it is only produced when doing actions such as blinking and raising eyebrows. Etiology: 1. Vascular factors In 1875, Schulitze et al. reported a case of HFS in which a “cherry” sized basilar artery aneurysm was found in the facial nerve area during autopsy. It is now known that approximately 80% to 90% of HFS is due to vascular compression of the facial nerve exiting the brainstem region. Clinical data suggest that the anterior inferior cerebellar artery (AICA) and posterior inferior cerebellar artery (PICA) are the predominant vascular factors causing HFS, while the superior cerebellar artery (SCA) is the next most common. It is known that the SCA originates from the junction of the basilar artery and the posterior cerebral artery and has the most constant course, whereas the PICA and AICA are relatively more variable and are prone to form vascular loops or ectopic compression of the facial nerve; in addition, the superior vagus artery and other large variant arteries such as the vertebral artery and the basilar artery may also cause compression of the facial nerve, resulting in HFS. In recent years, studies have shown that a single venous vessel can cause HFS when it compresses the facial nerve, and that both or more of these vessels can form a combined compression on the facial nerve, which to some extent affects the prognosis of HFS surgery. 2. Non-vascular factors Non-vascular occupying lesions of the pontocerebellar cerebellar angle (CPA), such as granulomas, tumors and cysts, can also produce HFS, which may be due to: 1) displacement of normal vessels due to occupancy. Singh et al. reported a case in which a CPA epidermoid cyst displaced the AICA and compressed the facial nerve; (2) direct compression of the facial nerve by the occupancy; and (3) the influence of the abnormal vessels of the occupancy itself, such as arteriovenous malformations, meningiomas, and aneurysms. In young patients, localized arachnoid thickening may be one of the main causes of HFS, while some congenital disorders such as Arnold-Chiari malformation and congenital arachnoid cyst may cause HFS. In young patients, localized arachnoid thickening may be one of the main causes of HFS, while some congenital disorders such as Arnold-Chiari malformation and congenital arachnoid cysts may occasionally produce HFS.3. Other factors The presence of compression in the region of the facial nerve outstem is the main cause of HFS, and most scholars have observed during pontocerebellar horn surgery that the presence of vascular compression in regions other than the facial nerve outstem does not produce HFS. Mar-tinelli also reported a case of HFS after injury to a peripheral branch of the facial nerve. In addition, HFS can also be seen in some systemic diseases such as multiple sclerosis. Only a few cases of familial HFS have been reported so far, and the mechanism is unknown, but it is presumed to be genetically related. Surgical treatment: Facial nerve microvascular decompression was pioneered by Jannetta in 1966. It is believed that the facial nerve root in the pontocerebellar peduncle area is compressed by the responsible vessel and becomes demyelinated, and the impulses between the afferent and efferent nerve fibers are short-circuited, resulting in facial muscle twitching. This theory and treatment method has been widely recognized with the advancement of current treatment methods and microsurgery techniques. Microvascular decompression of the facial nerve has become the best treatment for facial muscle twitching. The neurosurgery department of Beijing Tongren Hospital is the birthplace of neurosurgery in Beijing, established in 1953, where Academician Wang Zhongli and Professor Zhao Yadu worked. Since the re-establishment of the neurosurgery department in 1999, the statistics of Director Fu Jidi show that about 106 cases of facial nerve microvascular decompression have been performed, with an efficiency rate of 98.6%, which fully proves the effectiveness of facial nerve microvascular decompression. Ishikawa et al. studied the electrophysiology of the facial nerve during the perioperative period of microvascular decompression of the facial nerve for facial muscle twitching and concluded that the abnormal increase in excitability of the motor nucleus of the facial nerve caused by vascular compression was also one of the causes of facial muscle twitching, which could also explain the clear intraoperative vascular nerve decompression in two patients whose symptoms did not improve after surgery and gradually disappeared after several weeks, suggesting that the demyelination of the facial nerve needs time to repair.