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 the case of primary facial myospasm, it can occur even at rest, and the spasm is relieved after a few minutes and is not controlled; in the case of facial myospasm produced by the sequelae of facial palsy, it is only produced when doing actions such as blinking and raising eyebrows. 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 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, leading to HFS, which was previously thought to be due to pulsatile compression of the artery. In recent years, studies have shown that a single venous vessel can also cause HFS when compressing the facial nerve, and the above-mentioned vessels can form a joint compression of the facial nerve by both or more, which to some extent affects the prognosis of HFS surgery. 2, non-vascular factors Non-vascular occupying lesions in the pontocerebellar angle (CPA), such as granulomas, tumors and cysts, can also cause HFS, which may be due to: ① displacement of normal vessels due to the occupancy, Singh et al. reported a case of 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. (iii) The influence of the abnormal vessels of the occupancy itself such as arteriovenous malformation, meningioma, aneurysm, etc. In addition, some occupational lesions in the posterior cranial fossa may also cause HFS, such as a rare case of HFS due to compression of the facial nerve by a Chewang’s cell tumor of the middle nerve. Hirano reported a case of cerebellar hematoma in which the first symptom was 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 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.