Facial spasm (HFS) is a paroxysmal involuntary twitching of the hemifacial muscles, usually limited to one side of the face, hence the name hemifacial spasm, occasionally seen on both sides. It starts from the orbicularis oculi muscle and gradually develops to the cheek or even the whole face, and the reverse development is less common. It can be aggravated by fatigue and tension, especially when speaking and smiling, and can become spastic in severe cases. It mostly starts in middle age, with the youngest age reported to be two years old. In recent years, statistics have shown that the onset of HFS is independent of gender, and in a few cases, mild facial paralysis may develop. Some patients with primary facial myasthenia have a majority of onset after middle age, more often in women. In the early stages of the disease, the symptoms of facial myasthenia are mostly paroxysmal involuntary twitches of the orbicularis oculi muscle on one side of the face, which gradually and slowly extend to the other facial muscles on one side of the face, and the twitches of the corners of the mouth are the most noticeable. 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 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, 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, can also cause HFS due to: 1) displacement of normal vessels by the occupying site; 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 occupying site; 3) the influence of abnormal vessels in the occupying site itself, such as arteriovenous malformations, arteriovenous malformations, and cysts; and 4) the influence of abnormal vessels in the occupying site. The influence of abnormal blood vessels 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. 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 may be genetically related.