Delayed dyskinesia is divided into the following types according to the site of dyskinesia ① abnormal eye muscle movement: blinking, blepharospasm, etc.; ② abnormal facial muscle movement: facial muscle twitching, jerking and sad face, etc.; ③ abnormal mouth muscle movement: pouting, smacking, chewing, suction and lateral jaw movement, etc.; ④ abnormal tongue muscle movement: tongue extension, tongue contraction, wriggling and lip licking, etc.; ⑤ abnormal pharyngeal muscle movement: abnormal palate movement affecting pronunciation and (6) abnormal neck movement: slanting neck, backward neck, etc.; (7) abnormal trunk movement: uncoordinated trunk movement, odd posture, such as shrugging shoulders and retracting back, corkscrew, twisting spasm, diaphragm spasm producing grunting and breathing difficulties, sometimes the whole body swaying from side to side, repeated trunk flexion and extension, back and forth twisting, called body shaking sign; (8) abnormal limb movement: continuous flexion and extension of the distal limbs, called playing piano fingers (toes) sign. The proximal end is rarely involved, and a few of them show dance-like finger paddling movements, throwing movements, hand-foot twitch-like movements, repeatedly raising the hands or jumping on both legs. Some dopamine drugs such as levodopa, methyldopa, pacinin, and tranquilizers can also cause involuntary movements similar to TD. Occasionally seen in patients taking long-term antidepressants, anti-PD drugs, antiepileptic drugs and antihistamines, which are prone to occur with dose reduction or discontinuation. Associated factors include: (1) age and gender factors: the elderly are prone to occur and do not recover easily, more women than men; (2) patients with brain lesions are prone to use antipsychotics, and patients with negative symptomatic schizophrenia have an early age of onset and high incidence of TD; (3) drug factors: drug dose and duration of treatment are associated with the occurrence of TD, mostly seen in patients with Parkinson’s syndrome early in treatment. Pathogenesis The pathogenesis of delayed-onset dyskinesia is unclear, and damage to central dopaminergic neurons is one theory. Hypofunction of the GABAergic tract, neurotoxicity from free radicals, and direct neurological effects of antipsychotics have also been reported. It is generally believed that long-term administration of high-dose antipsychotics such as phenothiazines and butylphenols can block postsynaptic dopamine receptors (DR) for a long time, resulting in a feedback increase in presynaptic dopamine (DA) synthesis and release, increased sensitivity of postsynaptic DR to DA response, producing DR hypersensitivity, and being in a state of denervation sensitization, and physiological doses of DA can cause movement disorders, with levodopa or discontinuation of antipsychotics The physiological dose of DA can cause dyskinesia, which is consistent with the use of levodopa or discontinuation of antipsychotic drugs that often induce or worsen symptoms, and also supports that lisperdalin can reduce TD symptoms, haloperidol can temporarily mask symptoms, and DA potentiators can worsen symptoms. Pathological changes: Autopsy showed degenerative and atrophic nigrostriatal and caudate nuclei cells.