Facial muscle spasm (HSF) is a twitching of one side of the face (some people have bilateral spasms), and the more nervous and excited the spasm is, the more serious it becomes. The initial symptom of facial spasm is eyelid twitching, 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 forms and develops into facial spasm, which is linked to the corners of the mouth and, in severe cases, to the neck. It can be aggravated by fatigue and tension, especially when speaking and smiling. Eventually, a few cases may develop mild facial paralysis. Facial spasm can be divided into two types, one is primary facial spasm and the other is facial 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 only produced when doing actions such as blinking and raising eyebrows. The reasons for its occurrence are as follows: 1. Vascular factors: It is currently known that about 80% to 90% are due to the presence of vascular compression in the area of the facial nerve out of the brainstem. Clinical data show that the anterior inferior cerebellar artery (AICA) and posterior inferior cerebellar artery (PICA) are the main vascular factors causing facial spasm, 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, studies have shown that a single venous vessel can also cause HFS when it compresses the facial nerve, and the above-mentioned vessels can form a joint compression of the facial nerve by both or more, which to a certain 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 produce 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; (3) the influence of abnormal vessels in the occupancy itself, such as arteriovenous malformations, arteriovenous malformations, and cysts; and (4) the influence of the facial nerve by the occupancy itself. (2) direct compression of the facial nerve by the occupancy; (3) influence of the occupancy itself with 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 some congenital disorders such as Arnold-Chiari malformation and congenital arachnoid cyst may occasionally produce HFS. 3. Other factors: The presence of compression in the exocortical region of the facial nerve 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 exocortical region of the facial nerve 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 not known. Clinical manifestations of facial muscle spasm The initial stage of the disease is mostly paroxysmal involuntary twitching of the orbicularis oculi muscle on one side, which gradually and slowly extends to other facial muscles on one side of the face, and the twitching of the corners of the mouth muscle is the most noticeable, and in severe cases, it may even involve the ipsilateral broad neck muscle, but the frontalis muscle is less involved. The degree of twitching varies, and it is paroxysmal, rapid and irregular twitching. The initial twitch is light and lasts for only a few seconds, and then gradually grows for several minutes or longer, while the interval is gradually shortened and the twitches gradually increase in frequency. In severe cases, it is tonic, causing the ipsilateral eye to be unable to open, the corner of the mouth to be skewed to the ipsilateral side and unable to speak, often aggravated by fatigue, mental tension and voluntary movement, but it cannot imitate or control its seizure by itself. A convulsion can last from a few seconds to more than 10 minutes, with intervals of variable length. The patient feels distracted and unable to work or study, which seriously affects the patient’s physical and mental health. Most of the convulsions stop after sleep. Bilateral lateral muscle spasms are rarely seen. If there is, it is often started on both sides successively, and most of the convulsions stop on one side, then the other side has another attack, and the convulsions are light on one side and light on the other side, but the simultaneous onset and convulsions on both sides have not been reported. A few patients have mild facial pain during convulsions, and individual cases may be accompanied by ipsilateral headache and tinnitus. The intensity of spasms was graded according to Cohen et al. Grade 0: no spasm; Grade 1: increased transients or mild tremors of facial muscles caused by external stimuli; Grade 2: spontaneous mild tremors of eyelids and facial muscles without dysfunction; Grade 3: marked spasm with mild dysfunction; Grade 4: severe spasm and dysfunction, e.g., the patient is unable to read and has difficulty walking alone because he cannot keep his eyes open. Neurological examination is not positive for signs other than paroxysmal twitching of facial muscles. A small number of patients may have mild paralysis of the affected facial muscles in the late stage of the disease. The treatment of facial muscle spasm The diagnosis of facial muscle spasm is best not to acupuncture, because the disease itself is afraid of stimulation, sometimes acupuncture will aggravate the disease, some people at the time to see the effect, but later relapse will be powerful. The effect of taking carbamazepine or phenytoin sodium, which are anti-sedative and anti-epileptic drugs, is also not ideal, and the side effects of long-term use are also great. Botulinum toxin type A is also only controlled, generally playing a shot can control the longest one year, or six months to three months, long time injection will produce resistance, and because botulinum toxin type A only paralyze the nerves of the face caused by artificial facial paralysis, so at that time after playing facial muscle spasm will be controlled. However, patients who have been injected for a long time will have more or less facial paralysis. Surgical treatment of this disease is more ideal than the above methods. It is now clear that the majority of facial muscle spasms are caused by blood vessels compressing the facial nerve root. Therefore, the use of microvascular decompression is the best treatment for the cause. A C-shaped incision is made in the posterior hairline under general anesthesia, with a bone window of approximately 62.5 px, lateral to the posterior border of the sigmoid sinus and superior to the transverse sinus, and a dural “⊥”-shaped incision, with sutures draped over the superior border of the bone window. The cerebellum is gently lifted from the base of the posterior cranial fossa, the arachnoid membrane of the lateral pool of the medulla cerebellaris is sharply cut, and the posterior group of cranial nerves is brought forward, and the cerebellar choroid plexus above the Luschka foramen is lifted to reveal the facial nerve ventral to the auditory nerve; if the choroid plexus is well developed and obstructs the operating field, this part of the cerebellar tissue should be removed to avoid excessive stretching. If the vascular collaterals are lifted to reveal the obvious vascular pressure at the root of the facial nerve in the brainstem, it can be confirmed that this is the responsible vessel.