Facial muscle spasm, also known as facial muscle twitching or clonic facial muscle spasm, is characterized by twitch-like contraction of one side of the face, and is more common in middle-aged women. Etiology: Ectopic excitation or pseudo-synaptic conduction of the facial nerve. Surgical exploration reveals that the facial nerve root is compressed by blood vessels in most patients, which can be cured after microvascular decompression, suggesting a similar pathogenic basis with trigeminal neuralgia. 2. Clinical manifestations: The onset of the disease often starts with slight twitching of the muscles around the eyes and gradually expands to the muscles of the lower half of the face, especially the twitching of the corners of the mouth is obvious. In severe cases, the whole facial muscles may spasm, and may be accompanied by mild facial muscle weakness or muscle atrophy. The spasm may be aggravated by mental stress, fatigue, or voluntary movement, and disappears during sleep. Facial muscle spasm is not accompanied by pain, and the random contraction of facial muscle is generally unaffected during non-facial muscle spasm. 3. Diagnosis and differential diagnosis: According to the clinical manifestations, the diagnosis is generally not difficult, but needs to be differentiated from the following diseases: functional blepharospasm: occurs in elderly women, often bilateral, without lower facial muscle twitching. Habitual tics: occurring mostly in children and young adults, often with more pronounced muscle contractions, and associated with psychiatric factors. 4, treatment a, medication: treatment can be used carbamazepine 0.1 g twice a day, the dose can be gradually increased to 0.6 g / day, for mild cases can have some effect. b. Facial nerve branch block: The mechanism of treatment is to destroy the nerve function in different degrees to achieve certain therapeutic effect, which is symptomatic treatment, not treatment for the cause. The subcutaneous facial nerve branch block can be performed with 50% alcohol or facial nerve stem injection of 0.3~0.4 ml, which can stop the spasm and produce different degrees of facial muscle paralysis. Injection of botulinum toxin A into the affected facial muscle interferes with the release of neurotransmitters (acetylcholine) from the nerve endings, which can cause temporary weakness or facial paralysis of the muscles at the injection site and can maintain the therapeutic effect for 3-5 months, and can be repeatedly injected after relapse. c. Microvascular decompression: Because the pathogenesis of this disease is mainly caused by ectopic vascular compression of the facial nerve root, facial muscle spasm will disappear if the blood vessels compressing the nerve are separated from the nerve by surgical means. This method is to treat the cause of the disease, and the microvascular decompression of the facial nerve under electrophysiological monitoring carried out by the Beijing Institute of Functional Neurosurgery makes the surgery more effective and the complications are significantly reduced. The effective rate of facial spasm is 95%, and the recurrence rate is 5-10%. The indications for this surgery are: a. Frequent and severe facial muscle spasm attacks, affecting daily work and life; b. The disease has unsatisfactory results by other therapies, or recurrence after treatment.