The disease was first described by French neurologist Henry Meige in 1910 and was thought to be caused by secondary regeneration of facial nerve errors, which was further elaborated two years later and named Meige’s syndrome. syndrome. It usually starts slowly with a sensation of irritation or discomfort in one or both eyes, increased blinking frequency, and dry eyes before developing into blepharospasm. Symptoms worsen with fatigue, sunlight irritation, gaze, and stress, diminish when the mind is focused on something other than blepharospasm, and disappear during sleep. Most patients have paroxysmal blepharospasm as the first symptom. Blepharospasm is dominated by contraction of the orbicularis oculi muscle and contraction of the frontal and nasal muscles centered between the eyebrows, manifested by increased transients and tearing, and a few develop functional blindness after 1 to 2 years, eventually developing into severe bilateral blepharospasm, difficulty opening the eyes, and even loss of self-care. In some patients, the eyelid spasm gradually progresses to the lower face, showing symmetrical irregular and hyperactive contraction of the mandibular muscles of the mouth, which can prevent chewing, swallowing and speaking. (Tricks’ phenomenon). Symptoms often stop developing within six months to two years, but there is great individual variability in the rate of progression, with some reaching maximum severity within a few weeks of onset and others showing slow progression over 10 years. Approximately 1/3 of patients with Meige syndrome have been reported to have psychiatric symptoms such as depression, but the mechanism is unknown. Treatment of Meige’s disease: I. Pharmacotherapy: Currently, the main choices are cholinergic inhibitors (e.g., Antan, benztropine, dimethylacetamide, etc.), dopaminergic inhibitors (e.g., permethrin, haloperidol, thiamphenicol, etc.), GABA-enhancing drugs (Valium, nitroprusside, sodium valproate, etc.), and antipsychotics (e.g., fenadine, alprazolam, etc.). Evaluation of pharmacological therapy: Pharmacological therapy is effective in Meige syndrome, but there is no specific drug, because the pathogenesis is not clear, the existing drugs can not fundamentally change the pathological state. The limitation of drug therapy is that some patients have heavy adverse reactions, and this has no significant benefit to improve the quality of life of patients. Local injection of botulinum toxin A: Botulinum toxin A is injected locally to block the inward flow of calcium ions and inhibit the release of acetylcholine from nerve endings to relieve spasticity. A retrospective study over the past 10 years has shown that the overall effectiveness of local injections of botulinum toxin A for blepharospasm is about 90%. Botulinum toxin A is diluted to the desired concentration and injected intramuscularly into the orbicularis oculi, temporalis, and buccalis muscles, where electromyographic stimulation or electromyography is useful for precise localization. Injections are usually given at 10-18 sites at a dose of 2. 5-5 U per site. Additional injections can be given within 1 week in cases of residual spasticity at a total dose of 30-75 U. In cases of recurrence, repeat injections should be given at intervals of 4 months or more. Efficacy evaluation of local injection of botulinum toxin A: The treatment process is simple and the efficacy is more accurate. Disadvantages include: 1. high relapse rate: the effect usually lasts for about 3-6 months, and the treatment needs to be repeated within 6 months after the first injection. 2. multiple repeat treatments or short-term continuous injections, the efficacy of the treatment is reduced, and it should be noted that the interval between injections should be more than 4 months. This method has not been tested in a large scale double-blind controlled trial due to ethical limitations and is symptomatic treatment. The Pain Center of the Aviation General Hospital of China Medical University and the Meijer Disease Research Unit of the Institute of Translational Medicine of the Chinese Academy of Sciences in Beijing, led by Jianxiong An, has applied repeated injections of botulinum toxin in small doses to not only reduce side effects but also to achieve the desired outcome. Electroconvulsive therapy: The clinical efficacy of electroconvulsive therapy for meige is certain, and the recurrence rate is low, but at present, the clinical reports of electroconvulsive therapy for meige are all single cases, and no large sample clinical studies have been reported. The Pain Center of Aviation General Hospital of China Medical University and the Research Unit of Meige Disease of Beijing Institute of Translational Medicine of Chinese Academy of Sciences, led by Jianxiong An, applies painless ultrashort wave electroconvulsive therapy, which not only allows patients to receive electroconvulsive therapy under anesthesia without pain and memory, but also applies ultrashort wave stimulation to effectively prevent the side effects of previous electroconvulsive therapy affecting memory. Deep brain electrical stimulation: Deep brain electrical stimulation is a new technique for the treatment of Meige syndrome, which means that electrodes are implanted in specific parts of the brain for continuous stimulation to regulate muscle tone. The implantation sites include pallid bulb electrical stimulation and thalamic nucleus electrical stimulation. Evaluation of the efficacy of deep brain electrical stimulation: In addition to injury, bleeding, and infection, the most prominent complication of the procedure is the new onset of limb dysfunction, such as limitation of writing, typing, and walking, which is mild and acceptable to most patients. These complications occur in conjunction with the relief of lid-oral and mandibular symptoms, for which there is no specific treatment. Deep brain electrical stimulation is currently the most promising treatment for Méige syndrome, but more research is needed to guide its clinical application.