1. Menstrual epilepsy Dynamic changes in estrogen and progesterone during ovulation or non-ovulation or during menstruation can alter neuronal excitability and epileptiform seizure frequency. Acetazolamide, clobazam (CLB) or hormonal therapy (anti-estrogen or progesterone supplementation) may be used. Acetazolamide is a weak carbonic anhydrase inhibitor with mild diuretic and antiepileptic effects, but has the potential to cause mild transient metabolic acidosis. Usually the daily dose of 250-1000 mg is divided into 2 doses and taken in intermittent therapy, i.e. 10-14 days during the epileptic seizure susceptibility period, but should not be used in pregnant women. 2. Polycystic ovary syndrome (PCOS) Epileptic seizures interfere with the release of hormones from the hypothalamus and pituitary gland, and antiepileptic drugs can also cause disturbance of sex hormone levels. About 30% of women with epilepsy have polycystic ovaries compared to 15% of controls. Valproate (VPA) is associated with polycystic ovaries, hyperandrogenism, hyperinsulinemia, and obesity. 60% of women with epilepsy treated with VPA have polycystic ovaries compared to 20%-30% of those treated with other antiepileptic drugs, with the highest incidence in those taking VPA before age 20. After discontinuation, VPA-related signs and symptoms are mostly reversible. 3. Epileptic seizures during pregnancy It has been observed that in pregnant women with prior epilepsy, about 20%-33% have increased seizures, 7%-25% have decreased seizures, and 50%-83% have no significant change. The factors affecting this are sex hormone concentration, metabolism of AED, change in sleep habits, patient compliance with medication, and the presence of new stressful events (e.g., failed marriage, economic distress, etc.). Generalized tonic clonic seizures during pregnancy can lead to hypoxia and acidosis in both mother and fetus, increasing maternal and fetal mortality. It has been reported that various types of epileptic seizures in mothers during the first trimester cause fetal malformations up to 12.3%, while the rate of fetal malformations in mothers without epileptic seizures is only 4%. Therefore, the blood concentration should be monitored before pregnancy, every 3 months after pregnancy, and the last 4 weeks before delivery to adjust the AED in time, and the free level should be measured for AED with high or moderate protein binding rate. 4. Fetal antiepileptic drug syndrome Fetal antiepileptic drug syndrome refers to a combination of different clinical manifestations associated with chronic toxic reactions to antiepileptic drugs and contains fetal in utero growth retardation, severe congenital malformations, minor developmental abnormalities, microcephaly, cognitive dysfunction, and infant death. Minor anomalies are developmental variants or deviations that do not pose a threat to health, with an incidence of 6-20%, and manifest as distal finger (toe) and nail bed hypoplasia, and cephalofacial malformations such as wide eye spacing, wide nasal bridge, short arched nose, internal canthus, ear anomalies, and low hairline. Severe anomalies are anomalies of important anatomical structures at birth that significantly interfere with organ function and require intervention and correction, with an incidence of 1.25%-11.5%, including cleft lip, cleft palate, congenital heart disease (e.g., atrial septal defect, tetralogy of Fallot, ventricular septal defect, aortic constriction, patent ductus arteriosus, pulmonary valve stenosis) and neural tube defects (e.g., spina bifida and anencephaly). The incidence of genitourinary defects (e.g., hypospadias) is 4 to 6 percent. Many conventional drugs such as benzodiazepines, phenytoin sodium (PHT), carbamazepine (CBZ), phenobarbital (PB), and VPA are teratogenic. the incidence of neural tube defects in the first month of pregnancy was 0.5-1% in the CBZ-treated group and l-2% in the VPA-treated group, 10 and 20 times higher, respectively, than in the general population. a comprehensive analysis of 5 prospective studies showed that The absolute risk of neural tube defects due to VPA monotherapy can be as high as 3.8%, especially in mothers with VPA doses above 1000 mg per day with an increased risk. Additional collaborative studies have highlighted the importance of VPA dose. The teratogenicity of AEDs, except for VPA and CBZ, does not differ significantly. However, it is particularly clear that the risk of fetal antiepileptic drug syndrome increases with the type of antiepileptic drug taken, with the greatest risk of fetal malformation with exposure to multiple drugs and high doses, occurring well within the first trimester of pregnancy. The incidence of severe malformations in infants of women treated with more than four AEDs is approximately 25%. the teratogenic mechanism of AEDs is hypothesized to be due to the binding of free radical intermediates produced by the drugs to ribonucleic acid, disrupting DNA synthesis and organ development. High levels of oxidative metabolites are associated with a high risk of fetal malformations, and the teratogenic susceptibility of oxidative associations is genetically determined. Folate deficiency is also a possible mechanism for the teratogenicity of PHT, CBZ, PB and VPA. Women of childbearing age taking AED should be aware that: (1) 0.4-5 mg of folic acid should be taken daily; and (2) the lowest effective dose of the most efficacious and best tolerated monotherapy for the type of episode should be used before gestation, if possible. If there is a past history or family history of neural tube defects, avoid VPA, CBZ or consider switching to an antiepileptic drug other than CBZ or VPA in advance. (3) Maternal blood alpha-fetoprotein and amniotic fluid alpha-fetoprotein and acetylcholinesterase should be checked in the 15th-22nd weeks of gestation, and ultrasound examination in the 16th-20th weeks can detect neural tube defects at a rate of more than 95%. (4) Vitamin K1 10mg orally daily in the last month of pregnancy and vitamin K lmg intramuscularly or intravenously in the newborn at delivery to avoid bleeding due to antiepileptic drug-related Vit K deficiency and Vit K-dependent coagulation factor reduction.