I. Overview: Meige syndrome is a restrictive dystonia disorder.Meige syndrome belongs to adult ADHD and was first reported by French neurologist Meige in 1910. The main manifestation is bilateral eyelid spasm, facial dystonia-like involuntary movements, also known as eyelid spasm a mouth of jaw dystonia. Marsdan divided it into three types: (1) Blepharospasm type (BS): manifests as paroxysmal involuntary tightening-like spasmodic jerking or involuntary blinking of both eyelids. (2) Blepharospasm combined with oromandibular dystonia (BS-OMD): In addition to eyelid spasm, the mouth, lips and maxillofacial muscles also contract spastically, showing pouting, lip contraction, mouth opening, tongue extension, and involuntary twitching of the corners of the mouth and facial muscles, and the patient shows bizarre expressions. (3) OMD: only spasmodic twitching of the mouth, lips and jaw muscles. Clinical manifestations: The disease usually starts in old age, mostly in 40-70 years old, mostly in women, with a male:female ratio of 1:2-3. It usually starts slowly, with a sense of irritation or discomfort in one or both eyes, shyness and increased blinking frequency, and dry eyes before the onset, and later develops into blepharospasm. The 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, with contraction of the frontal and nasal muscles centered between the eyebrows, manifested by increased transients and tearing, and a few develop functional blindness after 1-2 years, eventually developing into severe bilateral blepharospasm, difficulty opening the eyes, and even loss of self-care. Some patients start with eyelid spasms and gradually progress to the lower face, showing symmetrical irregular and hyperactive contractions of the mandibular muscles of the mouth. Eye lid involvement: In mild cases, eye discomfort, dry eyes, photophobia, and increased transients may be manifested, and some cases may be misdiagnosed as “conjunctivitis”; in more severe cases, there may be episodes of difficulty in closing and opening the eyes, requiring the use of fingers to open the eyelids; in severe cases, functional blindness may result. Mouth-mandibular involvement: Involuntary mouth opening, mouth closing, pouting, lip retraction, cheek biting, tongue biting, and tooth bruxism. Neck muscle involvement: Discomfort in the neck, sloping neck, head shaking, head tilting back, shrugging shoulders, etc. In severe cases, it is difficult to maintain normal head position. Other: Involvement of tongue muscles may show involuntary movements such as tongue retraction or tongue extension, tongue twisting or tongue root tightening and stiffness; involvement of pharynx may show pharyngeal discomfort, coughing, slurred pronunciation and difficulty in swallowing; involvement of frontal muscles may show forehead tightening and frowning; involvement of hands and feet and limbs may show postural tremor, writing spasm, foot inversion and involuntary twitching; involvement of chest and abdomen may show local involuntary twitching with chest tightness and breath-holding. One of the characteristics of Meige syndrome is the dramatic reduction of symptoms seen when yawning, eating, coughing, singing, playing the piano, quizzing, playing the harmonica, or playing the mouth flute (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 their most severe level within a few weeks of onset and others showing a slow progression over 10 years. It has been reported that about 1/3 of patients suffering from Meige syndrome have psychiatric symptoms such as depression, but the mechanism is unknown. Diagnosis and differential diagnosis: 1. The diagnosis of the disease can be made mainly on the basis of the clinical features such as symmetrical and irregular contractions of the eyelid spasm and/or orofacial muscles, Tricks phenomenon, and disappearance during sleep. 2. Electrophysiological examination of the transient reflex shows an increase in the frequency of transients, a significant increase in the amplitude of the Rl component (reflecting the monosynaptic reflex) and the R2 component (reflecting the polysynaptic reflex), and a prolongation of the time limit of the electrically evoked corneal reflex. Differential diagnosis: When early symptoms of Meige syndrome are atypical, it should be differentiated from dry eye. The disease should also be differentiated from facial muscle spasm, tardive dyskinesia, orofacial dyskinesia, senile ptosis, functional perioral or eyelid hyperactivity, myasthenia gravis, tremor palsy, temporomandibular joint syndrome, neurosis, etc. V. Etiology and pathogenesis: The etiology and pathophysiological mechanisms of Meige syndrome are still unclear. Most scholars believe that the pathogenesis of the disease may be related to damage to the basal ganglia of the brain, hypofunction of nigrostriatal γ-aminobutyric acidergic neurons leading to dopaminergic receptor hypersensitivity or imbalance of dopamine transmitters and imbalance of cholinergic action. It has been reported that the disease is associated with the use of certain medications, such as long-term use of psychostimulants, anticonvulsant paralytics, and anxiolytics. It has also been reported that the disease is associated with reduced cortical inhibition due to environmental factors and genetic susceptibility. An autoimmune association has also been reported. Studies have also shown that facial trauma, including dental surgery, can cause oromandibular dystonia, which is particularly pronounced in people prone to infection. VI. Treatment: The disease is currently treated symptomatically. Treatment methods include oral medication, surgical treatment, local injection of botulinum toxin type A, etc. 1, conservative medical treatment: oral drugs include: (1) dopamine receptor antagonists, such as haloperidol, Tebrile, inosine, etc.; (2) γ-aminobutyric acid drugs, such as Jiajing Valium, sodium valproate, etc.; (3) anticholinergic drugs, such as Antan, etc.; (4) tranquilizers, such as diazepam, clonazepam, etc.; (5) antidepressants, such as amitriptyline, alpren, etc. 2, type A botulinum toxin local injection treatment: type A botulinum toxin can not restore the cortical motor area and the ventral side of the pre-motor area damaged motor activity, but can make the local facial muscle movement caused by enhanced somatosensory activity partially normalized, indicating that type A botulinum toxin may have some significance to the recovery of brain function in this disease. type A botulinum toxin effect lasts for weeks to months, the main complication is local muscle paralysis. The drug is injected into the eyelids, perioral area and related areas of the face. About 30% of patients can have relief. 3, stereotactic minimally invasive surgical treatment: for drug treatment is ineffective or less effective, or drug side effects are obvious, the patient’s symptoms obviously serious impact on life, neurosurgical intervention is also a more effective treatment options. The most advanced international treatment method is deep brain nucleus stimulation surgery (DBS), which is minimally invasive, reversible, adjustable and personalized, and is a safer and effective treatment with fewer side effects. The real point is that it is currently more expensive. For patients with poorer economic conditions, there is also the option of deep brain nucleus stereotactic disruption surgery. Our hospital is one of the first few hospitals in China to perform this type of surgery, and the efficacy is around 75-85%. However, the treatment of Meige syndrome is basically symptomatic, and there is a lack of specific methods for its eradication in domestic and foreign research.