Episodic movement-induced dyskinesia, also known as episodic movement-induced choreiform tardive dyskinesia in the past, is the most common type of episodic movement disorder and is clinically characterized by sudden movement-induced motor or postural abnormalities, such as brief and frequent episodes of dystonia, tardive dyskinesia, choreiform movements, and throwing-like movements. Because the disease is rare and the interictal period is normal, it can easily be misdiagnosed. 1. Etiology: PKD can be divided into primary and secondary. (1) Most of the primary cases have clear family history and conform to autosomal dominant mode of inheritance with episomal incompleteness, and there are also disseminated cases. The causative gene is localized on chromosome 16, and the current clear PKD1 type is due to PRRT2 gene, of which c.649dupC mutation is the mutation hotspot of PKD1 in China, which is about 60%. Combined with the results of our testing at Ruijin Hospital, we found that there are many family lines with incomplete epizootics, where one of the parents carries the mutation but does not develop the disease and passes it on to the child, who develops the disease, and since many are now only children, this appears as an epidemic, but is in fact still due to heredity. (2) Secondary PKD is seen in multiple sclerosis, traumatic brain injury, cerebrovascular disease, perinatal hypoxic encephalopathy and hyperthyroidism, diabetes mellitus, hypocalcemia and other metabolic abnormalities. 2. Clinical features: PKD mostly develops in adolescence, mostly in males, and mainly occurs when there is a sudden change in posture, direction of movement or force load. About 70% of patients complain of “aura” before the attack, such as numbness, coldness, tightness and heaviness in the affected limb. Most of them are unilateral, some of them are bilateral, and a few of them are alternating. When the facial or jaw muscles are involved, it may affect the speech and strange facial expressions. The seizures last from a few seconds to 10 seconds and usually do not exceed 5 minutes. PKD seizures are frequent and many patients have nearly 20 seizures per day, especially in adolescence, which can be as high as 30 to 100, and can gradually decrease after the age of 20. In 2004, Bruno et al. proposed the latest diagnostic criteria for PKD after analyzing the clinical data of 121 patients: (1) involuntary movements induced by sudden movements; (2) each attack usually lasts no more than 1 minute; (3) no loss of consciousness and no pain during the attack (4) Normal neurological examination and exclusion of other diseases; (5) Effective antiepileptic drug treatment, especially phenytoin sodium or carbamazepine; (6) No family history of the onset of the disease is usually between 1 and 20 years old. (4) Differential diagnosis: (1) Seizure non-motor induced dyskinesia: triggered by a variety of factors, such as coffee, alcohol, fatigue, etc., and not triggered by sudden movement, symptoms are similar to PKD, the duration can be several minutes to several hours, but the seizure frequency is low, only 1 to 3 times a day, and there can be an interval of several months. the MR-1 gene is its causative gene. (2) Dyskinesia due to seizure hypermobility: symptoms occur in association with prolonged or excessive movement, such as walking and running, most often involving the movement of the feet, and antiepileptic drugs are largely ineffective. (3) Paroxysmal ataxia: can be triggered by sudden motor stimulation, but mainly manifests as impairment of motor coordination function and balance function, often accompanied by postural tremor of the head and hands and fine twitching of facial and hand muscles. 5. Treatment: PKD generally responds better to antiepileptic drug therapy, especially carbamazepine and phenytoin sodium. Combining our experience with many PKD patients, our recommended treatment of choice: Deltodopa (carbamazepine) 50 mg to 100 mg every night at bedtime. Some patients require 200 mg and a change of medication if there are side effects such as skin allergies. Other antiepileptic drugs such as lamotrigine, oxcarbazepine, and tupilate can also be used with satisfactory results.