Benign pediatric epilepsy with central temporal spikes (BECTS), also known as Rolandic epilepsy, is classified as primary epilepsy by the International Society Against Epilepsy and is a relatively common partial seizure in childhood. The population prevalence is 2l/100,000, accounting for 15% to 24% of all childhood epilepsies, and the age of onset is 3 to 13 years, with 75% of patients having an onset between the ages of 5 and l0. Pediatric benign epilepsy is a kind of partial seizure with age and gradually disappears with age. We use a combination of Chinese medicine and Western and Chinese medicine to treat these children with good results. Benign focal pediatric epilepsy refers to a group of epilepsy syndromes with clinical manifestations of focal seizures, occurring at a specific age, with characteristic EEG manifestations, good response to antiepileptic drug therapy, and a good prognosis. The pathogenesis of pediatric benign focal epilepsy is generally considered to be closely related to genetic factors, and the sites and mutant forms of several types of epileptic gene mutations have been identified. Seizures occur as a result of abnormal gene regulation that causes dysfunction of ion channel transport, neurotransmitters, or their receptors, leading to a disturbance in the balance of excitatory and inhibitory loops between neurons in the developing brain and an abnormal increase in excitability of local neurons. The pediatric brain is highly plastic, and with age and the development of neuromediators and their receptors, the brain gradually undergoes modification and functional adjustment of neural networks within the brain, and eventually most of them can reach a new, relatively stable equilibrium state, and the seizures are terminated. Benign pediatric epilepsy with central temporal spikes (BECTS) is the most common type of benign focal pediatric epilepsy, accounting for 15-20% of pediatric epilepsy. The age of onset is 3-13 years (2-14 years have also been reported), with 76% of children having an onset between the ages of 5 and 10 years, with the most frequent onset between the ages of 8 and 10 years. Some authors have summarized the age profile of the disease in two sentences: “onset within 10 years of age and cessation within 20 years of age”. The disease is more frequent in boys than in girls. The disease is genetically related, with 30% of children having a family history of epilepsy, 15% of siblings having seizures with central temporal spikes, and 19% having central temporal spikes without clinical seizures. 11% of children have parents who had seizures as children that resolved in adulthood. Although the disease has a clear genetic predisposition, the site of the genetic abnormality and its nature have not yet been determined. A chain analysis of 22 core pediatric benign epilepsy families with central temporal spikes revealed that 70% of the families were linked to the chromosome 15q14 locus, which may be associated with the n acetylcholine receptor (nACh) 22 subunit. The clinical features of the disease are as follows: 1. Seizures are closely related to sleep: about 3/4 of children have seizures only during sleep, 15% may have seizures during sleep and wakefulness, and only 10%-20% have seizures only during wakefulness. Most of the seizures occur within 0.5-1 hour after going to sleep, some children have seizures before and after waking up, and some children have seizures during naps. If the seizure occurs during wakefulness, the child may experience abnormal sensation in the oropharynx, painful sensation in the inner side of the cheek or pharynx, or choking sensation. More common is motor seizures, which may be characterized by continuous swallowing movements or tonic contractions of the tongue muscles, inability to open the lower jaw, and inability to speak. Families often notice a lateral myoclonic jerk followed by (or simultaneous) ipsilateral limb jerking. Most children generalize to a full-blown tic, and sometimes the progression from a focal seizure to a full-blown seizure is so brief that the child’s parents do not observe a focal seizure but only a full-blown seizure. The number of seizures varies greatly, with 10%-20% of children having only one seizure, some children having more frequent seizures at the beginning, and then 1-2 seizures per year, and only 6%-20% of cases having more frequent seizures. EEG abnormalities: The background activity of the EEG is normal, but single or clustered spikes or spines may appear in the central temporal region. The abnormal discharges are closely related to sleep, and about 25-30% of children have abnormal spike-wave emission only during sleep. When the disease is suspected and the awake EEG is normal, a sleep EEG should be performed. Sometimes, the same child may show a change in the position of the spikes from one side to bilateral or contralateral in two EEG recordings, but there is no change in clinical symptoms. Sometimes it also shows bilateral synchronous spike-and-slow wave bursts. 4, neurological examination and imaging examination is normal: There are no abnormal signs in neurological examination, CT and MRI are normal, some organic changes may appear in individual children, but these changes cannot explain the clinical symptoms. 5. Good prognosis: Convulsions of this disease only appear in pediatric period, 50% of children stop after 3 years of seizures, 92% of children stop seizures at the age of 12 years, and 99% stop seizures at the age of 17 years. The EEG returns to normal slowly, about 2 years after the termination of the seizure, and most of them return to normal at the age of 17-19 years. The child’s intelligence is normal. Regarding the treatment of the disease, since about 10% of children have only one seizure, there is no urgency to treat the first seizure and treatment can be started when another seizure occurs. However, for children who have had multiple episodes or a persistent state at the time of consultation, medication should be started as soon as the diagnosis is clear. The disease responds well to medications, and most children have good results with sodium valproate, phenobarbital, phenytoin sodium, carbamazepine, or topiramate. Generally, after 2 years of medication control, even if the EEG has not returned to normal, the medication can be gradually reduced, and the reduction process takes about 6 months to 1 year, and then the medication is discontinued. In some cases, treatment is more difficult. The prognosis of this disease is good, and the key is to recognize the disease and diagnose it correctly. Treatment is not difficult and does not require high doses of medication or multi-drug combination therapy.