Hemifacial spasm (HFS), also known as facial twitching. It is a condition of involuntary twitching of the face on one half of the face. The twitching is paroxysmal and irregular, with varying degrees, and can be aggravated by fatigue, stress and voluntary movements. The onset of the twitching usually starts from the orbicularis oculi muscle and then involves the whole face. The disease occurs mostly after middle age and is commonly seen in women. The cause of this disease is unknown, and modern Western medicine lacks a specific treatment for it. At present, symptomatic treatment is generally used, but the effect is not ideal. Facial muscle spasm is a twitch on one side of the face (individuals appear bilateral spasms), the more nervous and excited the more serious the spasm. As the initial symptom of facial myospasm is eyelid jumping, folk have the name of “left eye jumping for money, right eye jumping for disaster”, so generally do not attract people’s attention, after a period of time the foci formed, the development of facial myospasm, linked to the corner 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 uncontrolled; in facial myospasm produced by the sequelae of facial palsy, it is produced only when doing actions such as blinking and raising the eyebrows. 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 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 second. 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 therefore 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, it has been 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. Non-vascular factors Non-vascular occupying lesions in the pontocerebellar angle (CPA), such as granulomas, tumors, and cysts, may also cause HFS due to: (1) displacement of normal vessels by the occupancy; Singh et al. reported a case of a CPA epidermoid cyst that displaced the AICA and compressed the facial nerve, resulting in HFS; (2) direct compression of the facial nerve by the occupancy; and (3) the influence of abnormal vessels in the occupancy itself. Such as arteriovenous malformation, meningioma, aneurysm, etc. 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 congenital disorders such as Arnold-Chiari malformation and congenital arachnoid cysts may occasionally produce HFS. Other factors The presence of compression in the region of the facial nerve out of the brainstem is the main cause of HFS, and most authors have observed during pontocerebellar horn surgery that the presence of vascular compression in the region outside the facial nerve out of the brainstem does not produce HFS. Mar-tinelli also reported a case of HFS after injury to a peripheral branch of the facial nerve, and further investigation is needed to determine whether the presence of compression factors in areas other than the brainstem region of the facial nerve leads to HFS.