Facial muscle spasm, also known as facial twitch, is an episodic, recurrent, involuntary twitching of the facial muscles innervated by the facial nerve. The incidence of facial muscle twitching: trigeminal neuralgia = 1:2.8 according to preliminary domestic statistics. I. Etiology Facial myoclonus is still divided into two categories: primary and secondary. Secondary facial myospasm refers to those whose etiology is clear, such as peripheral facial palsy caused by some facial nerve trauma or facial neuritis, which can cause facial myospasm during the recovery period; some tumors of the pontocerebellar angle or skull base arachnoiditis involving the facial nerve root can also cause the occurrence of this disease. The pathogenesis of primary facial myospasm is the same as that of primary trigeminal neuralgia, which is thought to be caused by abnormal vascular compression of the facial nerve root out of the pontocerebellar segment, resulting in demyelination of the nerve and “short-circuiting” of the current between nerve fibers. In recent years, a large number of clinical practices have also shown that once the compression of the nerve root by the blood vessel is released, facial muscle spasm can be stopped immediately or gradually. Most of the facial muscle spasms are limited to one side, often occurring first in the lower eyelid, and then gradually expanding in scope, spreading to the corners of the mouth, other facial muscles and broad neck muscles after 1 to 2 years. There is no aura before the attack, and the attack is characterized by rapid and frequent muscle twitching for a few seconds to a few minutes each time, with everything as normal in the interval. The seizures can be triggered by voluntary facial movements and chewing, transient eyes or random facial expressions, and can be aggravated by emotional excitement, stress, exertion or prolonged reading time, while the symptoms are reduced when resting or emotionally stable. In severe cases, twitching may continue throughout the day or even during sleep. In some patients, the eyelid fissures may become smaller due to compulsive contraction of the eyelids, and in some patients, even the facial muscles may contract tensely, causing the corners of the mouth to be continuously tilted to the side of the disease. The disease has a chronic course and can extend over many years, affecting the patient’s work, spirit and life to a certain extent. The electromyographic examination of facial muscle can find high amplitude F and abnormal muscle response waveform when electromyographic examination is performed in patients with facial muscle spasm; stimulation of the mandibular branch of facial nerve can induce the muscle potential of orbicularis oculi muscle; electromyographic monitoring during microvascular decompression of facial nerve reveals that once the blood vessels compressing the facial nerve are separated, the abnormal facial electromyogram can disappear. 2, imaging examination 2.1 CT, MRI and other examinations: can make a clear diagnosis of secondary facial myospasm caused by some occupational and organic lesions. 2.1 Magnetic resonance tomographic angiography (MRA): This examination technique can show the relationship between cerebral blood vessels and cranial nerves, which can help to diagnose primary facial muscle spasm caused by vascular compression of facial nerve. Treatment For primary facial spasm, it is usually difficult to control the seizures with drugs. In the past, various destructive methods were used to treat the disease by causing partial paralysis of the facial muscles, such as alcohol closure, percutaneous puncture facial nerve radiofrequency thermal coagulation, facial nerve branch or trunk mostly severed, intracranial facial nerve extrusion, facial nerve canal nerve partial injury, etc. In recent years, with the development of primary facial muscle spasm, the facial nerve has been partially damaged. In recent years, with the clarification of the cause of primary facial spasm, microvascular decompression of the facial nerve root has become the preferred surgical treatment method. For those who are too old for surgery or unwilling to undergo surgery, the use of botulinum toxin A (botulinum toxin A) closure also has certain efficacy. Facial nerve root microvascular decompression Facial nerve root microvascular decompression has become the preferred surgical treatment method This method, the surgery from the posterior cranial fossa access, exposure of the affected pontocerebellar angle, the facial nerve root at the beginning of the pontocerebellar segment to find the compressed blood vessels, to confirm the free, and then filled with Tefleon cotton ball, so that the blood vessels and nerve separation. Postoperatively, spasticity can be controlled in more than 90% of patients. The key to achieving definitive results is adequate decompression of the responsible vessel and avoiding the omission of the responsible vessel. With the introduction of neuroendoscopic techniques, the cure rate has now been increased to more than 95%. 2. Botulinum toxin A closure treatment This method is also commonly used nowadays, especially for those with blepharospasm. Botulinum toxin A is injected into the branches of the main facial nerve to cause partial facial muscle paralysis, but does not affect the overall facial activity. A single injection can last for 3 to 4 months, and the closure can be repeated after a relapse, but permanent facial paralysis may result after too many closures.