1. lamotrigine (LTG) As a broad-spectrum antiepileptic drug, LTG’s mechanism of action is to block voltage-dependent sodium channels and reduce the release of excitatory amino acids. Its protein binding rate is 55%, half-life is 15-30h, and 90% is cleared by the liver. Common side effects include ataxia, dizziness, diplopia, drowsiness, headache, convulsions, and insomnia. Serious toxic effects include rash, Stevens Johnson syndrome, and toxic epidermal necrolysis, as well as hepatic and renal failure, disseminated intravascular coagulation (DIC), and hypersensitivity reactions such as arthritis. Karande et al. reported a case of anticonvulsant hypersensitivity syndrome (AHS) induced by LTG use and confirmed in vitro by tests. Cunnington found that the teratogenicity of LTG was similar to that of other AEDs, at about 2.9%. However, the sample size is small and needs to be confirmed by further studies. Enzyme-induced AEDs such as phenytoin and CBZ increase clearance when combined with LTG, while the enzyme inhibitor VPA decreases clearance of LTG by about 60%. No other new AEDs have been found to have a significant effect on clearance of LTG, but there is an increased chance of side effects when combined. Contraceptives can reduce the blood concentration of lamotrigine, and no interaction with cytochrome P450 and warfarin has been observed. 2. Oxcarbazepine (OXC) Its mechanism of action is to block voltage-dependent sodium channels, with a protein binding rate of 40%, half-life of 4-9h, and hepatic clearance of 70%. Common side effects are drowsiness, dizziness, headache, ataxia, nausea, vomiting, diplopia, blurred vision, vertigo, low blood sodium, and rash. Studies have found that the likelihood of hyponatremia increases with age in patients. Previous studies have shown that pregnant women taking oxcarbazepine monotherapy for epilepsy have not shown an increased incidence of malformations in their offspring. oXC may increase PHT or PB blood levels. No interaction between OXC and erythromycin has been seen. OXC reduces contraceptive, ethinyl estradiol, and felodipine serum concentrations, decreases 25-OHD serum concentrations, and affects other bone metabolism markers to some extent [6]. 3. topiramate (TPM) A broad-spectrum antiepileptic drug whose mechanism of action includes blocking voltage-dependent sodium channels, enhancing γ-aminobutyric acid (GABA) receptors, and blocking AMPA-type glutamate receptors. The protein binding rate is 9-17%, half-life is 15-23h, 40-70% is cleared by kidney, and some is metabolized by liver. Side effects such as kidney stones, glaucoma, metabolic acidosis, weight loss, speech impairment, drowsiness, fatigue, nausea, loss of appetite, weight loss, abnormal sensation, slow and confused reaction, vertigo, hypohidrosis, headache, etc. are common. Notably, about 48% of patients with TPM-induced metabolic acidosis do not exhibit clinical symptoms [7]. As for the effect of TPM on cognitive function, the findings are inconsistent and further studies are needed.TPM decreases the serum concentrations of lithium, digoxin, and ethinyl estradiol, decreases contraceptive efficacy, and increases flupredinol serum concentrations. Inhibition of CYP 2C19 leads to a decrease in plasma concentrations of PHT. Some reports have shown that the use of TPM in pregnant women can lead to fetal malformations [8]. 4. gabapentin (GBP) The mechanism of action is unclear and may act by increasing the amount of γ-aminobutyric acid (GABA) in the brain. Protein binding is 0, half-life is 4-6h, 100% is cleared by the kidneys, and absorption is dose-dependent. The main side effects are weight gain, peripheral edema, behavioral changes common in children, and viral infections. It is worth noting that patients with renal failure are prone to neurotoxicity-based side effects of GBP, which can lead to myoclonus and coma in severe cases. A small sample study found that the concentration of GBP in cord blood was 1.3-2.1 times higher than maternal blood concentration, and the milk/maternal blood gabapentin concentration ratio was 1 from 2 weeks to 3 months after delivery, suggesting active placental transport of GBP, but no serious side effects were observed in infants as a result of maternal GBP administration. No significant interactions were seen with warfarin and contraceptives, and there are no reported results of its interactions with other antiepileptic drugs. 5. levetiracetam (LEV) The mechanism of action is not yet clear. It is not protein bound, has a half-life of 6-8h, 66% is cleared by the kidneys, 34% is hydrolyzed by the acetamide group, is not metabolized by the liver, and does not induce hepatic enzyme synthesis. No serious side effects have been observed. The main side effects are irritability and behavioral changes. No interactions with other antiepileptic drugs have been observed. Studies have found that the addition of LEV for the treatment of focal epilepsy resulted in improvements in cognitive function, particularly in attention and oral fluency. It is suggested that LEV may affect the metabolism of attentional, verbal areas and thus improve neurological function.