Hypotonia-paralytic dyskinesia: it involves the head, neck and lumbar region, such as the neck is too soft to lift the head, the lumbar region is too soft to straighten and project the abdomen, and the walking is too weak to step and lift the legs and feet to drag the ground. This is a clinical manifestation of tardive dyskinesia. Delayed-onset movement disorder, also known as delayed hyperactivity disorder persistent movement disorder, induced by antipsychotic drugs, is a persistent stereotyped repetitive involuntary movements Crane (1968) first suggested that it is the most serious and problematic extrapyramidal reaction caused by antipsychotic drug treatment occurs at a fairly high rate. So what is the pathogenesis of soft neck inability to raise the head? Here is a brief description. The pathogenesis of the cause of tardive dyskinesia is unclear, with damage to central dopaminergic neurons being one theory. Hypofunction of the GABAergic tract, neurotoxicity from free radicals, and direct action of antipsychotic drugs on the nervous system 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 the postsynaptic DR to DA responses, resulting in DR hypersensitivity and a denervated sensitized state, 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.