Meige syndrome is a dystonic disorder. It is mainly characterized by bilateral blepharospasm and involuntary facial dystonia-like movements, also known as blepharospasm-oral mandibular dystonia. It was first reported by French neurologist Henri Meige in 1910, and Marsdan classified it into three types: (1) blepharospasm; (2) blepharospasm combined with oromandibular dystonia; and (3) oromandibular dystonia. The onset of the disease is usually slow, with irritation or discomfort in one or both eyes, photophobia, increased blinking frequency, and dry eyes, and later develops into blepharospasm. Symptoms worsen with fatigue, sunlight irritation, gaze, and stress, and decrease when the mind is focused on something other than blepharospasm, and disappear during sleep. Some patients start with blepharospasm and progress to the lower face, showing symmetrical irregular and hyperactive contractions of the mandibular muscles of the mouth. Tension of the mandibular muscles may prevent chewing, swallowing, and speaking, and spasmodic dysphonia and dyspnea may occur when the laryngeal and respiratory muscles are invaded, and blepharospasm may lead to functional blindness in severe cases. One of the characteristics of Meige syndrome is the dramatic reduction of symptoms when yawning, eating, coughing, singing, playing the piano, quizzing, playing the harmonica, or playing the mouth flute (Tricks’ phenomenon). The symptoms often stop developing within 6 months to 2 years, but the rate of progression is highly variable, ranging from a few weeks after the onset of the disease to a slow progression over 10 years. The diagnosis is based on clinical features such as eyelid spasms and/or symmetrical, irregular contractions of the orofacial muscles, Tricks’ phenomenon, and disappearance during sleep. When early symptoms of Meige syndrome are atypical, it can be easily confused with 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, and neurosis. The etiology and pathophysiological mechanisms of Meige syndrome are unknown. 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 dopamine transmitter imbalance, and imbalance of cholinergic action. It has been reported that the disease is associated with the use of certain pharmacogenic sources, such as long-term use of psychostimulants, anticonvulsant paralytics, and anxiolytics. There are also reports that tend to link the disease to environmental factors that promote and genetic susceptibility resulting in decreased cortical inhibition. It has also been shown that facial trauma, including dental surgery, can cause suboral collar dystonia, which is particularly pronounced in susceptible populations. The disease is currently treated symptomatically. Treatment includes oral medications, surgical procedures, and local injections of botulinum toxin type A. Oral drugs include: (1) dopamine receptor antagonists, such as haloperidol, Tebrile, etc.; (2) anticonvulsants, such as sodium valproate, carbamazepine, levetiracetam, etc.; (3) anticholinergics, such as Antan, etc.; (4) tranquilizers, such as diazepam, clonazepam, etc.; (5) antidepressants, such as amitriptyline, etc. (6) muscle relaxants such as baclofen may have some effect. It is still difficult to cure. Chinese medicine considers this disease belongs to the category of wind evidence. Treatment should be based on nourishing the liver and kidneys, quenching the wind, resolving phlegm and stopping spasm, and supplemented by the method of tranquilizing the mind. In the early stage, the disease can be treated with seven-leaf Shenan tablets and whole Tianma capsule.