Facial muscle spasm is also known as facial muscle twitching. It is a condition of involuntary twitching of the half side of the face. The twitches are paroxysmal and irregular, with varying degrees of intensity, and may be aggravated by fatigue, mental 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 more nervous and excited the spasm is, the more severe it becomes. The initial symptom of facial myospasm is eyelid jumping, which is also known as “left eye jumping for money, right eye jumping for disaster”, so it usually does not attract people’s attention, but after a period of time, the lesion will develop into facial myospasm, which is linked to the corners of the mouth and, in severe cases, the neck. Facial muscle spasm can be divided into two types, one is primary facial muscle spasm, and the other is 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 in the resting state, 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 produced only when doing actions such as blinking and raising eyebrows. Its etiology is mainly divided into vascular factors, non-vascular factors and other factors. Vascular factors It is currently known that approximately 80-90% of HFS is due to the presence of vascular compression in the area of the facial nerve exiting the brainstem. Clinical data indicate that the anterior inferior cerebellar artery (AICA) and posterior inferior cerebellar artery (PICA) are predominant among the vascular factors causing HFS, while the superior cerebellar artery (SCA) is 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. 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 due to the occupancy 2. direct compression of the facial nerve by the occupancy; 3. 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 can also lead to HFS, such as the rare HFS caused by compression of the facial nerve by a Chewang’s cell tumor of the median nerve. Other factors The presence of compression in the region of the brain stem exiting the facial nerve is the main cause of 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 not known, presumably related to genetics. Treatment 1, drug therapy: In addition to phenytoin sodium or carbamazepine and other drugs may be effective for some light patients, general central sedative drugs, inhibitors and hormones are not significantly effective. 2.Radiofrequency temperature-controlled thermal coagulation therapy 3.Microvascular decompression surgery treatment can remove the root cause of the disease and treat the disease from the cause, with an efficiency of 99%.