Facial muscle spasm, also known as facial muscle twitching, is a paroxysmal involuntary twitching of the hemifacial muscles, the cause of which is still unclear and usually limited to one side of the face. Most of the patients have intermittent twitching of the eye muscles, which gradually spreads to other parts of one side of the face. In severe cases, half of the face is in spasm and cannot open the eyes, which can cause facial pain, headache, tinnitus and other symptoms. Facial twitching is often obvious when meeting strangers or when showing their faces in public places. It seriously affects the patient’s daily life. Facial muscle spasm treatment: Facial muscle spasm treatment includes drugs, acupuncture, botulinum toxin injection and several other methods, the effect is not ideal, some clinics advertise that acupuncture or physical therapy and other how many courses can cure facial muscle spasm, are not credible. At present, microvascular decompression is the most effective method of treatment, with a success rate of 95% and a recurrence rate of less than 5%. If there are facial twitching episodes, which affect work and life, you should go to the hospital in time and consider microvascular decompression surgery after diagnosis. The etiology of facial spasm is still unknown. The main theories are: ① Microvascular compression theory. In 1962, it was proposed that facial myospasm and trigeminal neuralgia may be caused by mechanical compression of blood vessels, and in 1967, experts in the study of this theory, after the successful experience of microvascular decompression in the posterior cranial fossa to treat facial myospasm, believed that microvascular compression of nerves is the cause of the disease, which was supported by many people. This theory suggests that damage to the facial nerve may occur when the facial nerve and microvessels form a mutually perpendicular straddling intersection during their travels, which may be mechanically compressed by this vessel. Since the facial nerve exits the brainstem area, which is the transition zone between the central glial segment and the peripheral myelinated segment, it is very sensitive to microvascular compression. The most common vessels compressing the facial nerve in this zone are the inferior anterior cerebellar artery and its branches. When the facial nerve is compressed and the myelin sheath is damaged, the nerves are exposed and come into contact with each other, and nerve impulses are short-circuited, causing facial muscle spasm. ②The theory of facial nerve nucleus dysfunction. The facial nerve motor nucleus located in the pontocerebrum is subjected to various chronic stimuli, such as chronic inflammation and compression, during its journey out of the pontocerebrum, causing hyperexcitability of ganglion cells and opening the “abnormal synaptic connections” in the nucleus. Clinical manifestations The disease is more common in middle-aged women and occurs on one side of the face, and it is rare for both sides to be involved. (1) Paroxysmal involuntary twitching of one side of the facial muscles, mostly starting from the orbicularis oculi muscle and gradually spreading to the facial expression muscles including the broad neck muscle. ②The disease progresses slowly. At the beginning, the twitching is light and will be relieved in a short time, with a long interval, and then the seizures will become more frequent, and even tonic spasms of the lateral muscles, incomplete lid closure and “strange appearance” of lifting the corners of the mouth upward may appear. Late onset of ipsilateral facial muscle weakness can occur. (3) Facial muscle spasm is a sudden and irregular twitch that cannot be controlled by the patient and is caused or aggravated by exertion. One twitch is from a few seconds to a few minutes or longer, and the interval is gradually shortened with the increase of symptoms. In severe cases, the convulsions are tonic until the affected eye cannot be opened, and the patient is often distracted during the convulsions, which affects work and study. Most of the convulsions stop after sleep. ④ The face is usually painless during the convulsions, and there is no neck or limb twitching. ⑤ Individuals may have headache and ipsilateral tinnitus, auditory hypersensitivity, disturbance of vasodilation and contraction of the affected face, but no loss of vision. Several methods of treatment for facial muscle spasm such as drugs, acupuncture and botulinum toxin injection are not effective. At present, microvascular decompression is the best method of treatment, and the current efficiency is over 95%, and there are no obvious complications and sequelae.