(2) Myoclonus is easily induced by external stimuli, such as auditory, tactile, visual stimuli, or aggravated; (3) EEG with or without epileptiform electrical activity, brain imaging may not have specific lesions; (4) Treatment is preferred to valproic acid, clonazepam and other antiepileptic drugs; (5) Overall prognosis is good, possibly (5) The overall prognosis is good, but there may be residual neurological deficits. Post-hypoxic myoclonus is not uncommon in clinical practice and can occur after cerebral hypoxia from various causes, with cardiopulmonary resuscitation and asphyxia being its common causes. Myoclonus is the main clinical symptom and is characterized by rapid, transient, clustered contractions of a muscle or group of muscles or brief loss of muscle tone of the active muscles and twitching, easily induced by external stimuli, such as auditory, tactile, and visual stimuli (i.e., reflex myoclonus). According to the time of occurrence of post-hypoxia myoclonus can be divided into acute and chronic, the acute one is called myoclonic status, which occurs 24-48h after cardiac arrest, when the patient is comatose, and most patients show myoclonic epilepsy, which suggests a poor prognosis; the chronic one is called Lance-Adams syndrome, where myoclonus occurs after the patient regains consciousness, and it is mainly action myoclonus, and can be accompanied by It is thought to be caused by multifocal cortical activity, and the neurological deficits improve with time and have a good prognosis. About half of the patients often have epileptic seizure symptoms, and the EEG shows multi-source multi-focal damage, and about half of them can see epileptic discharges. Valproic acid, clonazepam, and levetiracetam are preferred for treatment, and a combination of drugs is recommended. It has also been reported that patients with refractory chronic post-hypoxic myoclonus have been greatly relieved by the use of sodium oxybutynate. The pathogenesis of post-hypoxic myoclonus is still not clear. It has been suggested that post-hypoxic myoclonus is caused by impaired 5-HT metabolism, mainly manifested by a decrease in 5-HT subtypes such as 5-HT1B, 5-HT2A, and 5-HT1D. Studies have shown that A receptors of GABA are involved in the pathogenesis of post-hypoxic myoclonus. Post-hypoxic myoclonus is a symptomatic myoclonus, and its diagnosis is mainly based on the history and typical clinical features. EEG may or may not have epileptic electrical activity; treatment is preferred with antiepileptic drugs such as valproic acid, clonazepam and levetiracetam. The long-term prognosis of the disease is good, with most patients experiencing significant remission of myoclonus after several years or a combination of mild neurological deficits. After awakening from the machine, the patient developed myoclonic seizures with dysarthria, ataxia, and seizures when exposed to light, which were not yet induced by sound stimulation, and his family could only blindfold him with a cloth all day. Treatment was LEV+VPA+CNZ.