The mechanism of action of antiepileptic drugs lies in their ability to inhibit the abnormal discharge of brain neurons and to stop the expansion of abnormal discharge in the brain. With regular medication, nearly 80% of patients’ seizures can be controlled, and eventually 50% of patients can be completely off medication. However, for a variety of reasons, many epileptic patients fail to receive proper medication, which seriously affects the patient’s normal activities, and repeated seizures can also affect intelligence or lead to trauma, and may cause death if persistent status epilepticus occurs. Therefore, proper antiepileptic drug treatment is important to control seizures, reduce secondary brain damage and improve the quality of patient’s survival. The reasons affecting the success or failure of drug therapy are many, and we know that ignoring pharmacokinetic factors is often an important reason for the failure of antiepileptic drug therapy or for some patients to be “untreated for a long time”. The first of these is that the brain neurons in epileptic patients discharge abnormally at random. The seizure is a transient brain dysfunction caused by abnormal and excessive hyper-synchronized discharge of brain neurons. It is characterized by the appearance of sudden and transient clinical symptoms. Except for special cases (e.g., when conducting a provocation test or certain epilepsies with a tendency to have periodic seizures), the timing of abnormal neuronal discharges is unpredictable and completely random. This important feature requires that the dose of the therapeutic drug used during drug treatment be “just right”, i.e., that the “effective concentration” to control abnormal discharges is always achieved (there is considerable individual variation), but that the concentration is not too low or too high. The dose is “just right”, i.e., it can always reach the “effective concentration” for abnormal discharge control (there are relatively large individual differences), and avoid the occurrence of adverse reactions due to too low concentration that cannot play a therapeutic role or too high concentration. To achieve this, the number of daily doses and the duration of dosing need to be reasonably arranged according to the pharmacokinetic characteristics of the antiepileptic drugs used in each patient to ensure that the antiepileptic drugs always reach a stable blood concentration. It is easy to understand why patients with poor medication compliance or patients who sometimes forget to take their medication are likely to experience seizures as a clinical phenomenon. 2. All antiepileptic drugs have their pharmacokinetic characteristics. Each antiepileptic drug has its own half-life (T 1/2), for example, phenobarbital is up to 96 ± 12 hours, compared with about 47 hours in infancy, while valproate is 8-10 hours, carbamazepine 8-12 hours, and in between, Tolteride (topiramate) 20-30 hours (15-20 hours in children). The half-life can help estimate the time for antiepileptic drugs to reach steady-state blood concentrations, which are generally reached approximately 5-7 half-lives after the effective dose is given. For example, sodium valproate and carbamazepine take about 3 days to reach steady-state blood concentrations, while phenobarbital takes about 20 days to reach steady-state blood concentrations. Antiepileptic drugs can only play their stable therapeutic role if they reach stable blood concentrations. In some patients with epilepsy, it is inappropriate to stop or change the medication because of seizures when the antiepileptic drug has not yet reached stable blood concentration. The number of daily doses should be reasonably arranged according to the pharmacokinetic characteristics. In principle, the number of doses should be arranged in such a way that the blood concentration reaches a steady state in 24 hours. In general, the dosing time should not exceed 1 half-life of the drug. The number of doses per day can be calculated according to the half-life of different drugs, such as carbamazepine and sodium valproate generic tablets preferably three times a day, and phenobarbital only once a day. Many of the newer antiepileptic drugs that have been introduced in recent years require only 2 doses per day because of their longer half-lives. In the case of controlled-release formulations of traditional drugs, the number of daily doses should be determined by their release rate. Unfortunately, it is common to see clinical cases where the number of daily doses is unreasonable and leads to “prolonged treatment”, such as when only one daily dose of sodium valproate generic or carbamazepine tablets is scheduled, or when two daily doses are scheduled and the dose is significantly insufficient. In such cases, the time when the patient has a clinical episode is often during the concentration trough at the end of the half-life of the drug. 4. Arrange and instruct the patient on the specific time to take the medication. As different antiepileptic drugs have different pharmacokinetic characteristics, even if the same antiepileptic drug also exists whether the controlled release dosage form. Therefore, proper scheduling of medication is an important means to ensure that antiepileptic drugs achieve stable blood concentrations and play a stable therapeutic role. Due to traditional habits and the different working hours of each person, in our clinical patients, the three daily doses are usually executed within 12 hours (7:00-12:00-19:00) by the patients themselves, which may lead to low blood levels in the early morning hours; some patients often forget to take the dose at noon, which may lead to low blood levels in the afternoon hours. As a result, these patients often describe seizures occurring in the early morning or afternoon. In this regard, if the clinician can carefully ask the patient about the specific time of each seizure and analyze its relationship with the time of medication, it is easy to identify and correct treatment failure due to inappropriate timing of medication. 5. When combining antiepileptic drugs, attention should be paid to the interactions between antiepileptic drugs. These include pharmacodynamic interactions and pharmacokinetic interactions. The former refers to two drugs with similar or opposing pharmacological mechanisms of action without alterations in plasma concentrations of the drug or/and its metabolites. The latter refers to a drug that interferes with the in vivo processes of another drug (including absorption, distribution, metabolism and excretion), altering the concentration of the drug at the site of action. Pharmacokinetic interactions are clinically important, e.g., carbamazepine may decrease the expected concentrations of valproate, phenytoin sodium, paromidone, lamotrigine, ethosuximide, and felbamate, but may increase the expected concentration of phenobarbital; valproate sodium may increase the expected concentrations of carbamazepine epoxide, paromidone, phenobarbital, lamotrigine, and ethosuximide; phenytoin sodium may decrease the expected concentrations of carbamazepine, valproate phenytoin sodium may decrease the expected concentrations of carbamazepine, sodium valproate, felbamate, lamotrigine and ethosuximide, but may increase the expected concentration of phenobarbital; phenobarbital may decrease the expected concentrations of carbamazepine, sodium valproate, felbamate, lamotrigine and ethosuximide; paromidone may decrease the expected concentrations of carbamazepine, sodium valproate, felbamate, lamotrigine and ethosuximide; aminolevulinic acid may decrease the expected concentrations of phenytoin sodium, phenobarbital and paromidone The expected concentration of lamotrigine may increase the expected concentration of carbamazepine epoxide; ethosuximide may increase the expected concentration of phenytoin sodium; felbamate may increase the expected concentration of phenytoin sodium, carbamazepine epoxide, sodium valproate and phenobarbital, etc. Therefore, when the newly added antiepileptic drug reduces the concentration of the original antiepileptic drug, it may lead to exacerbation of seizures, especially when the dose of the original antiepileptic drug is at the lowest effective dose. Therefore, for patients with epilepsy who are not well treated with antiepileptic drugs, after adding another antiepileptic drug, close attention should be paid to monitoring changes in drug concentration, observing clinical seizures and noting the occurrence of adverse drug reactions, and adjusting the drug dose according to the specific situation in a timely manner. 6. Special patients need special treatment. A very small number of epileptic patients have a certain pattern of seizures to be found, such as those who often have seizures during sleep or menstruation. For these patients with seizures that often occur at specific times, every effort should be made to achieve a peak concentration of the drug after absorption that will just cover this time period. For patients who are prone to an increased number of seizures during specific phases (e.g., menstruation), an increase in the dose of antiepileptic drugs may be considered during this period (with an appropriately earlier start of medication). 7. Blood levels should be monitored when available. Blood concentration monitoring can accurately reflect the individual patient’s metabolism of antiepileptic drugs. Several commonly used traditional antiepileptic drugs can be monitored clinically, providing an important means to comprehensively assess the efficacy of antiepileptic drugs, especially for guiding the treatment of refractory epilepsy. The reasons for changes in blood drug concentrations should be analyzed comprehensively, including age, drug half-life, medication compliance, diet, gastrointestinal and hepatic and renal function, and the interaction of coadministered drugs. The dose of antiepileptic drugs, the number of doses and the duration of dosing should be adjusted according to the changes in blood levels and the clinical seizures. For patients who have reached “effective” blood levels but still cannot control their seizures, the reasons for this should be carefully analyzed and, if necessary, a change of antiepileptic drugs should be considered. It should be noted that when seizures are well controlled, individual blood levels vary greatly. For patients with seizure types that are easier to control and for patients with a low frequency of seizures before treatment, relatively low blood levels can control seizures. On the other hand, sometimes the upper limit of the therapeutic range is not absolute, because some patients need to be in this high concentration range to achieve the desired control, for example, in some patients, the blood concentration of sodium valproate reaches 120ug/ml to completely control the clinical seizures. Therefore, as long as there are no adverse effects, the upper limit of this therapeutic range is the “effective” blood concentration for the patient.