Facial muscle spasm, also known as facial muscle twitching. It is a condition of involuntary twitching of the half side 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 (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, folklore also has the name of “left eye jumping for money, right eye jumping for disaster”, so it usually does not cause facial myospasm. The people’s attention, after a period of time the foci formed, developed into facial muscle spasm, linked to the corners of the mouth, serious even with the neck. Facial myospasm can be divided into two types, one is the primary type of facial myospasm and the other is the facial myospasm 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 uncontrolled; in the case of facial myospasm produced by the sequelae of facial palsy, it is produced only when doing actions such as blinking and raising the eyebrows. Etiology Hemifacial spasm (HFS) is a paroxysmal involuntary jerking of the hemifacial muscles, usually confined to one side of the face, hence the name hemifacial spasm, occasionally seen on both sides. It starts in the orbicularis oculi muscle and gradually progresses to the cheek and even the whole face. 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, and the youngest age is reported to be two years old. In recent years, statistics have shown that the onset of HSF is independent of gender, and in a few cases, mild facial paralysis may develop. Vascular factors In 1875, Schulitze et al. reported a case of HFS in which a “cherry” sized basilar aneurysm was found at autopsy in the facial nerve. 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 indicate 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 variable 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 CPA epidermoid cyst that displaced the AICA and compressed the facial nerve, (2) direct compression of the facial nerve by the occupying site, and (3) abnormalities of the occupying site itself. The influence of 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. Other factors The presence of compression in the region of the facial nerve out of the brainstem is a major 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. 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, but it is presumed to be genetically related. Clinical manifestations Some patients with primary facial myasthenia have the onset of the disease after middle age, more often in women. The twitching of the corners of the mouth is the most noticeable, and in severe cases it may even involve the ipsilateral cervicalis muscle, but the frontalis muscle is less frequently involved. The degree of twitching varies, and it is paroxysmal, rapid and irregular twitching. The initial convulsion is light and lasts for only a few seconds, and then it gradually grows for several minutes or longer, while the interval is gradually shortened and the convulsions 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 the inability to speak, often aggravated by fatigue, nervousness, 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. Treatment The cause of facial muscle spasm is generally due to excessive fatigue, tension, dry fire, internal heat, and external wind and cold, according to traditional Chinese medicine. Western medicine says: blood vessels compressing the facial nerve later cause adhesions, facial nerve ischemia and hypoxia cause facial nerve spasm. Most of them are paroxysmal involuntary twitching of the hemifacial muscles, usually confined to one side of the face, hence the name hemifacial spasm, occasionally seen in both. It starts from the orbicularis oculi muscle and gradually progresses to the cheeks and even the whole face, and the reverse development is less common. It can be exacerbated by fatigue and tension, especially when speaking and smiling, and can become spastic in severe cases. It mostly starts in middle age, and the youngest age is reported to be two years old. Previously, it was thought to be more prevalent in females. In recent years, statistics have shown that the onset of the disease is independent of gender. In a few cases, mild facial paralysis may develop. If the diagnosis of facial spasm is confirmed, it is best not to use acupuncture, because the disease itself is afraid of stimulation, sometimes acupuncture will aggravate the disease, some people can see the effect at the time, but later relapse will be strong. In addition to taking carbamazepine or phenytoin sodium these anti-sedative anti-epileptic drugs only control, and long-term taking side effects are also very big, dependence is also relatively strong. The botulinum toxin type A is also only controlled, usually a shot can control the longest one year, or six months to three months, long time injection will produce resistance, and because the botulinum toxin type A only paralyzes the facial nerve caused by artificial facial paralysis, so at the 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 relatively more ideal than the two methods mentioned above, and more patients will adopt it. However, the recurrence rate is also very high. The most one patient has had four surgeries in clinical contact. At present, Western medicine treatment is no more than the above-mentioned methods. There are also many Chinese medicine treatments in China, most of which are mainly based on oral Chinese medicine, but most of the traditional oral medicine is simply to open the meridians, dispel the wind and resolve the problem, which will only be effective, but it is difficult to solve the problem at the root. The use of bee therapy has certain efficacy, but the treatment process is longer, persevere, can be expected to cure.