Facial muscle spasm is twitching on one side of the face (some people have bilateral spasms), and the more nervous and excited the spasm is, the more serious it is. As the initial symptom of facial myospasm is eyelid jumping, folk say “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, developed into facial myospasm, linked to the corner of the mouth, serious 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 in the resting state, 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 eyebrows. Facial muscle spasms are paroxysmal involuntary twitches of the hemifacial muscles, usually limited to one side of the face, and therefore also called hemifacial spasms, occasionally seen on both sides. It starts from the orbicularis oculi muscle and gradually develops to the cheeks and even the whole half of the face, and the reverse development is less common. It can be aggravated by fatigue and tension, especially when speaking and smiling, and in severe cases it can be spastic. It mostly starts in middle age, with the youngest age reported to be two years old. In the past, it was thought to be more prevalent in females, but in recent years, statistics have shown that the onset of the disease is not related to gender. a few cases of HSF may develop into mild facial paralysis at the end of the disease. 1. Vascular factors: It is known that about 80-90% of HFS is due to the presence of vascular compression in the brainstem area exiting the facial nerve. The SCA is known to originate from the junction of the basilar artery and the posterior cerebral artery and has the most constant course, while 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 variable large arteries such as the vertebral artery and the basilar artery may also form compression of the facial nerve, resulting in HFS. 2. Non-vascular factors: Non-vascular lesions of the pontocerebellar cerebellar angle (CPA) HFS can also be caused by the displacement of normal vessels due to the occupancy, direct compression of the facial nerve by the occupancy, and the influence of the abnormal vessels of the occupancy itself, such as arteriovenous malformations, meningiomas, and aneurysms. 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. 3. Other factors: The presence of compression factors 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 areas other than the exocortical region of the facial nerve does not produce 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 is presumed to be genetically related. Clinical manifestations of facial myasthenia Some patients with primary facial myasthenia develop it after middle age, more often in women. In the early stage of the disease, it is mostly paroxysmal involuntary twitching of the orbicularis oculi muscle on one side, which gradually and slowly expands to other facial muscles on one side of the face. 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 often starts on both sides successively, and most of the convulsions stop on one side and then the other side seizes again, and the convulsions are light on one side and light on the other side, and bilateral simultaneous onset and convulsions have not been reported. A few patients have mild facial pain during convulsions, and individual cases may be accompanied by ipsilateral headache and tinnitus. 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: pronounced 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 course of the disease.